Cerebral arteriovenous malformation (AVM)

Cerebral arteriovenous malformation (AVM)

Intracranial arteriovenous malformation in the brain.

see Cerebral arteriovenous malformation epidemiology.

see Arteriovenous malformation associated aneurysm

Cerebral microarteriovenous malformation

Parafalcine arteriovenous malformation,….

Ruptured cerebral arteriovenous malformation

Unruptured cerebral arteriovenous malformation

AVMs that occur in the coverings of the brain are called dural arteriovenous malformation.

Deep arteriovenous malformation.

Motor area arteriovenous malformation.

Pediatric Cerebral arteriovenous malformation.

Cerebral Arteriovenous Malformation Grading.

Cerebral arteriovenous malformation rupture risk.

Significant progress in the understanding of their pathogenesis has been made during the last decade, particularly using whole genome sequencing and biomolecular analysis 1)

Cerebral arteriovenous malformation pathophysiology

Cerebral Arteriovenous Malformation Clinical Features.

Primary lobar hemorrhages (usually due to cerebral amyloid angiopathy) are typically seen in elderly. Younger patients may also develop lobar haemorrhages, but in such cases they usually have an underlying lesion (e.g. cerebral arteriovenous malformation).

see Cerebral arteriovenous malformation treatment.

Cerebral arteriovenous malformation outcome.

Cerebral arteriovenous malformation complications.

Cerebral arteriovenous malformation case series.

Bhanot et al. presented a patient with intraparenchymal hemorrhage due to cerebral arteriovenous malformation (AVM) who exhibited acute ST segment myocardial infarction (STEMI) after neurosurgery. Serial cardiac biomarkers and echocardiograms were performed which did not reveal any evidence of acute myocardial infarction. The patient was managed conservatively from cardiac stand point with no employment of anticoagulants, antiplatelet therapyfibrinolytic agents, or angioplasty and recovered well with minimal neurological deficit. This case highlights that diffuse cardiac ischemic signs on the ECG can occur in the setting of an ICH after neurosurgery, potentially posing a difficult diagnostic and management conundrum 2).


1)

Vetiska S, Wälchli T, Radovanovic I, Berhouma M. Molecular and genetic mechanisms in brain arteriovenous malformations: new insights and future perspectives. Neurosurg Rev. 2022 Oct 11. doi: 10.1007/s10143-022-01883-4. Epub ahead of print. PMID: 36219361.
2)

Bhanot RD, Kaur J, Sriwastawa S, Bell K, Suchdev K. Postoperative ‘STEMI’ in Intracerebral Hemorrhage due to Arteriovenous Malformation: A Case Report and Review of Literature. Case Rep Crit Care. 2019 Apr 22;2019:9048239. doi: 10.1155/2019/9048239. PMID: 31231576; PMCID: PMC6507120.

Cerebral venous sinus thrombosis after Vaccine-induced Immune Thrombotic Thrombocytopenia

Cerebral venous sinus thrombosis after Vaccine-induced Immune Thrombotic Thrombocytopenia

Health care providers should be familiar with the clinical presentations, pathophysiology, diagnostic criteria, and management consideration of this rare but severe and potentially fatal complication of the SARS-COV2 vaccine


Cerebral venous sinus thrombosis (CVT) prior to the COVID pandemic was rare, responsible for 0.5 of all strokes, at the onset of the pandemic on the East Coast, overall cross-sectional imaging volumes declined due to maintaining ventilation, high levels of care and limiting disease spread, although COVID-19 patients have a 30-60 times greater risk of CVT compared to the general population, and vaccination is currently the best option to mitigate severe disease. In early 2021, reports of adenoviral vector COVID vaccines causing CTV and Vaccine-induced Immune Thrombotic Thrombocytopenia (VITT), led to a 39.65% increase in cross-sectional venography, however, in this study unvaccinated patients in 2021 had a higher incidence of CVT (10.1%), compared to the vaccinated patients (4.5%). Clinicians should be aware that VITT CVT may present with a headache 5-30 days post-vaccination with thrombosis best diagnosed on CTV or MRV. If thrombosis is present with thrombocytopenia, platelets <150 × 109, elevated D-Dimer >4000 FEU, and positive anti-PF4 ELISA assay, the diagnosis is definitive. VITT CVT resembles spontaneous autoimmune heparin-induced thrombocytopenia (HIT) and is postulated to occur from platelet factor 4 (PF4) binding to vaccine adenoviral vectors forming a novel antigen, anti-PF4 memory B-cells, and anti-PF4 (VITT) antibodies. 1).

Neurosurgical management involves treating intracranial hypertension however survival outcomes in a cohort were poor. In these series, decompression was performed in deteriorating patients however prophylactic decompression, in the presence of extensive venous sinus thrombosis, should be considered on a case-by-case basis. As vaccination programs accelerate across the world, neurosurgeons are likely to be increasingly involved in managing intracranial hypertension in patients with VITT-related sinus thromboses. 2).


A distinct clinical profile and a high mortality rate were observed in patients meeting the criteria for thrombocytopenia syndrome (TTS) after SARS-CoV-2 vaccination 3).


Non-heparin anticoagulants and immunoglobulin treatment might improve outcomes of VITT-associated cerebral venous thrombosis 4)

Sixty-two studies reporting 160 cases were included from 16 countries. Patients were predominantly females with a median age of 42.50 (22) years. AZD1222 was administered to 140 patients (87·5%). TTS onset occurred in a median of 9 (4) days after vaccination. Venous thrombosis was most common (61.0%). Most patients developed cerebral venous sinus thrombosis (CVST; 66.3%). CVST was significantly more common in female vs male patients (p = 0·001) and in patients aged <45 years vs ≥45 years (p = 0·004). The mortality rate was 36.2%, and patients with suspected TTS, venous thrombosis, CVST, pulmonary embolism, or intraneural complications, patients not managed with non-heparin anticoagulants or IVIG, patients receiving platelet transfusions, and patients requiring intensive care unit admission, mechanical ventilation, or inpatient neurosurgery were more likely to expire than recover. 5)

Cerebral venous thrombosis caused by vaccine-induced immune thrombotic thrombocytopenia (VITT-CVT) is a rare adverse effect of adenovirus-based SARS-COV2 vaccines. In March 2021, after autoimmune pathogenesis of VITT was discovered, treatment recommendations were developed. This comprised immunomodulation, nonheparin anticoagulants, and avoidance of platelet transfusion. The aim of the study was to evaluate adherence to these recommendations and their association with mortality.

Scutelnic et al. used data from an international prospective registry of patients with CVT after adenovirus-based SARS-CoV-2 vaccination. They analyzed possible, probable, or definite VITT-CVT cases included until 18 January 2022. Immunomodulation entailed the administration of intravenous immunoglobulins and/or plasmapheresis.

99 VITT-CVT patients from 71 hospitals in 17 countries were analyzed. Five of 38 (13%), 11/24 (46%), and 28/37 (76%) of patients diagnosed in March, April, and from May onwards, respectively, were treated in-line with VITT recommendations (p<0.001). Overall, treatment according to recommendations had no statistically significant influence on mortality (14/44 (32%) vs 29/55 (52%), adjusted OR 0.43 (95%CI 0.16-1.19)). However, patients who received immunomodulation had lower mortality (19/65 (29%) vs 24/34 (70%), adjusted OR 0.19 (95%CI 0.06-0.58)). Treatment with non-heparin anticoagulants instead of heparins was not associated with lower mortality (17/51 (33%) vs 13/35 (37%), adjusted OR 0.70 (95%CI 0.24-2.04)). Mortality was also not significantly influenced by platelet transfusion (17/27 (63%) vs 26/72 (36%), adjusted OR 2.19 (95%CI 0.74-6.54)).

In VITT-CVT patients, adherence to VITT treatment recommendations improved over time. Immunomodulation seems crucial for reducing mortality of VITT-CVT 6).


During a 2-week period, we encountered five cases presenting with a combination of cerebral venous thrombosis (CVT), intracerebral hemorrhage, and thrombocytopenia. A clinical hallmark was the rapid and severe progression of disease in spite of maximum treatment efforts, resulting in fatal outcomes for 4 out of 5 patients. All cases had received the ChAdOx1 nCov-19 vaccine 1-2 weeks earlier and developed a characteristic syndrome thereafter. The rapid progressive clinical course and high fatality rate of CVT in combination with thrombocytopenia in such a cluster and in otherwise healthy adults is a recent phenomenon. Cerebral autopsy findings were those of venous hemorrhagic infarctions and thrombi in dural venous sinuses, including thrombus material apparently rich in thrombocytes, leukocytes, and fibrin. Vessel walls were free of inflammation. Extra-cerebral manifestations included leech-like thrombi in large veins, fibrin clots in small venules, and scattered hemorrhages on skin and membranes. CVT with thrombocytopenia after adenovirus vectored COVID-19 vaccination is a new clinical syndrome that needs to be recognized by clinicians is challenging to treat and seems associated with a high mortality rate 7)

A patient was rapidly treated with steroids, immunoglobulin, and fondaparinux. She underwent within 6 h after hospital admission a mechanical thrombectomy in order to allow flow restoration in cerebral venous systems. Neuroendovascular treatment in cerebral venous thrombosis related to VITT has never been described before. It can represent a complementary tool along with the other therapies and a multidisciplinary approach 8).


Two cases of ChAdOx1 nCov-19 (AstraZeneca)-are associated with thrombotic thrombocytopenia syndrome (TTS) and cerebral venous sinus thrombosis (CVST). At the time of emergency room presentation due to persistent headache, blood serum levels revealed reduced platelet counts. Yet, 1 or 4 days after the onset of the symptom, the first MR-angiography provided no evidence of CVST. Follow-up imaging, performed upon headache refractory to nonsteroidal pain medication verified CVST 2-10 days after initial negative MRI. Both the patients received combined treatment with intravenous immunoglobulins and parenteral anticoagulation leading to an increase in platelet concentration in both individuals and resolution of the occluded cerebral sinus in one patient 9).


Rodriguez et al. reported the first described post Ad26.COV2.S (Janssen, Johnson & Johnson) vaccine-induced immune thrombocytopenia (VITT) case outside US. CASE DESCRIPTION: CA young woman without any medical history presented an association of deep vein thrombosis and thrombocytopenia at day 10 after vaccine injection. The patient was treated with low-molecular-weight heparin at a first medical institution. Twelve days post Ad26.COV2.S vaccination, the patient was admitted to the hospital for neurological deterioration and right hemiplegia. Medical imaging using MRI showed thrombosis of the major anterior part of the sagittal superior sinus with bilateral intraparenchymal hemorrhagic complications. Screening tests for antibodies against platelet factor 4 (PF4)-heparin by rapid lateral flow immunoassay and chemiluminescence techniques were negative. Platelet activation test using heparin-induced multiple electrode aggregometry confirmed the initial clinical hypothesis. Despite immediate treatment with intravenous immunoglobulin, dexamethasone, danaparoid, and attempted neurosurgery the patient evolved toward brain death.

Even though it is an extremely rare complication of vaccination physicians should maintain a high index of suspicion of VITT in patients who received an adenovirus-vector-based SARS-CoV-2 vaccine within the last 30 days with persistent complaints compatible with VITT or thromboembolic event associated with thrombocytopenia. The diagnosis should not be excluded if the rapid anti-PF4 immunological or chemiluminescence techniques yield negative results. An adapted functional assay should be performed to confirm the diagnosis. Early treatment with intravenous immunoglobulin and non-heparin anticoagulants is essential as delayed diagnosis and administration of appropriate treatment are associated with poor prognosis 10).


A case of VITT in a young female who presented 11 days after receiving the first dose of the Covishield vaccine, with severe headache and hemiparesis. She was diagnosed with CSVT with a large intraparenchymal bleed, requiring decompressive craniectomy and an extended period of mechanical ventilation.

The patient was successfully treated with intravenous immunoglobulin and discharged after 19 days in ICU. Although she was left with long-term neurological deficits, an early presentation and a multidisciplinary approach to management contributed to a relatively short stay in the hospital and avoided mortality 11).


1)

Franceschi AM, Petrover DR, McMahon TM, Libman RB, Giliberto L, Clouston SAP, Castillo M, Kirsch C. Retrospective review COVID-19 vaccine induced thrombotic thrombocytopenia and cerebral venous thrombosis-what can we learn from the immune response. Clin Imaging. 2022 Jul 15;90:63-70. doi: 10.1016/j.clinimag.2022.06.020. Epub ahead of print. PMID: 35926315; PMCID: PMC9283127.
2)

Eltayeb M, Jayakumar N, Coulter I, Johnson C, Crossman J. Decompressive craniectomy for intracranial hypertension in vaccine-induced immune thrombotic thrombocytopaenia: a case series. Br J Neurosurg. 2022 Aug 25:1-4. doi: 10.1080/02688697.2022.2115007. Epub ahead of print. PMID: 36004613.
3)

Sánchez van Kammen M, Aguiar de Sousa D, Poli S, Cordonnier C, Heldner MR, van de Munckhof A, Krzywicka K, van Haaps T, Ciccone A, Middeldorp S, Levi MM, Kremer Hovinga JA, Silvis S, Hiltunen S, Mansour M, Arauz A, Barboza MA, Field TS, Tsivgoulis G, Nagel S, Lindgren E, Tatlisumak T, Jood K, Putaala J, Ferro JM, Arnold M, Coutinho JM; Cerebral Venous Sinus Thrombosis With Thrombocytopenia Syndrome Study Group, Sharma AR, Elkady A, Negro A, Günther A, Gutschalk A, Schönenberger S, Buture A, Murphy S, Paiva Nunes A, Tiede A, Puthuppallil Philip A, Mengel A, Medina A, Hellström Vogel Å, Tawa A, Aujayeb A, Casolla B, Buck B, Zanferrari C, Garcia-Esperon C, Vayne C, Legault C, Pfrepper C, Tracol C, Soriano C, Guisado-Alonso D, Bougon D, Zimatore DS, Michalski D, Blacquiere D, Johansson E, Cuadrado-Godia E, De Maistre E, Carrera E, Vuillier F, Bonneville F, Giammello F, Bode FJ, Zimmerman J, d’Onofrio F, Grillo F, Cotton F, Caparros F, Puy L, Maier F, Gulli G, Frisullo G, Polkinghorne G, Franchineau G, Cangür H, Katzberg H, Sibon I, Baharoglu I, Brar J, Payen JF, Burrow J, Fernandes J, Schouten J, Althaus K, Garambois K, Derex L, Humbertjean L, Lebrato Hernandez L, Kellermair L, Morin Martin M, Petruzzellis M, Cotelli M, Dubois MC, Carvalho M, Wittstock M, Miranda M, Skjelland M, Bandettini di Poggio M, Scholz MJ, Raposo N, Kahnis R, Kruyt N, Huet O, Sharma P, Candelaresi P, Reiner P, Vieira R, Acampora R, Kern R, Leker R, Coutts S, Bal S, Sharma SS, Susen S, Cox T, Geeraerts T, Gattringer T, Bartsch T, Kleinig TJ, Dizonno V, Arslan Y. Characteristics and Outcomes of Patients With Cerebral Venous Sinus Thrombosis in SARS-CoV-2 Vaccine-Induced Immune Thrombotic Thrombocytopenia. JAMA Neurol. 2021 Nov 1;78(11):1314-1323. doi: 10.1001/jamaneurol.2021.3619. PMID: 34581763; PMCID: PMC8479648.
4)

Perry RJ, Tamborska A, Singh B, Craven B, Marigold R, Arthur-Farraj P, Yeo JM, Zhang L, Hassan-Smith G, Jones M, Hutchcroft C, Hobson E, Warcel D, White D, Ferdinand P, Webb A, Solomon T, Scully M, Werring DJ, Roffe C; CVT After Immunisation Against COVID-19 (CAIAC) collaborators. Cerebral venous thrombosis after vaccination against COVID-19 in the UK: a multicentre cohort study. Lancet. 2021 Sep 25;398(10306):1147-1156. doi: 10.1016/S0140-6736(21)01608-1. Epub 2021 Aug 6. PMID: 34370972; PMCID: PMC8346241.
5)

Waqar U, Ahmed S, Gardezi SMHA, Tahir MS, Abidin ZU, Hussain A, Ali N, Mahmood SF. Thrombosis with Thrombocytopenia Syndrome After Administration of AZD1222 or Ad26.COV2.S Vaccine for COVID-19: A Systematic Review. Clin Appl Thromb Hemost. 2021 Jan-Dec;27:10760296211068487. doi: 10.1177/10760296211068487. PMID: 34907794; PMCID: PMC8689609.
6)

Scutelnic A, Krzywicka K, Mbroh J, van de Munckhof A, Sánchez van Kammen M, Aguiar de Sousa D, Lindgren E, Jood K, Günther A, Hiltunen S, Putaala J, Tiede A, Maier F, Kern R, Bartsch T, Althaus K, Ciccone A, Wiedmann M, Skjelland M, Medina A, Cuadrado-Godia E, Cox T, Aujayeb A, Raposo N, Garambois K, Payen JF, Vuillier F, Franchineau G, Timsit S, Bougon D, Dubois MC, Tawa A, Tracol C, De Maistre E, Bonneville F, Vayne C, Mengel A, Michalski D, Pelz J, Wittstock M, Bode F, Zimmermann J, Schouten J, Buture A, Murphy S, Palma V, Negro A, Gutschalk A, Nagel S, Schoenenberger S, Frisullo G, Zanferrari C, Grillo F, Giammello F, Martin MM, Cervera A, Burrow J, Garcia Esperon C, Chew BLA, Kleinig TJ, Soriano C, Zimatore DS, Petruzzellis M, Elkady A, Miranda MS, Fernandes J, Hellström Vogel Å, Johansson E, Philip AP, Coutts SB, Bal S, Buck B, Legault C, Blacquiere D, Katzberg HD, Field TS, Dizonno V, Gattringer T, Jacobi C, Devroye A, Lemmens R, Kristoffersen ES, Bandettini di Poggio M, Ghiasian M, Karapanayiotides T, Chatterton S, Wronski M, Ng K, Kahnis R, Geeraerts T, Reiner P, Cordonnier C, Middeldorp S, Levi M, van Gorp ECM, van de Beek D, Brodard J, Kremer Hovinga JA, Kruip MJHA, Tatlisumak T, Ferro JM, Coutinho JM, Arnold M, Poli S, Heldner MR. Management of cerebral venous thrombosis due to adenoviral COVID-19 vaccination. Ann Neurol. 2022 Jun 10. doi: 10.1002/ana.26431. Epub ahead of print. PMID: 35689346.
7)

Wiedmann M, Skattør T, Stray-Pedersen A, Romundstad L, Antal EA, Marthinsen PB, Sørvoll IH, Leiknes Ernstsen S, Lund CG, Holme PA, Johansen TO, Brunborg C, Aamodt AH, Schultz NH, Skagen K, Skjelland M. Vaccine Induced Immune Thrombotic Thrombocytopenia Causing a Severe Form of Cerebral Venous Thrombosis With High Fatality Rate: A Case Series. Front Neurol. 2021 Jul 30;12:721146. doi: 10.3389/fneur.2021.721146. PMID: 34393988; PMCID: PMC8363077.
8)

Mirandola L, Arena G, Pagliaro M, Boghi A, Naldi A, Castellano D, Vaccarino A, Silengo D, Aprà F, Cavallo R, Livigni S. Massive cerebral venous sinus thrombosis in vaccine-induced immune thrombotic thrombocytopenia after ChAdOx1 nCoV-19 serum: case report of a successful multidisciplinary approach. Neurol Sci. 2022 Mar;43(3):1499-1502. doi: 10.1007/s10072-021-05805-y. Epub 2022 Jan 10. PMID: 35001190; PMCID: PMC8743093.
9)

Braun T, Viard M, Juenemann M, Struffert T, Schwarm F, Huttner HB, Roessler FC. Case Report: Take a Second Look: Covid-19 Vaccination-Related Cerebral Venous Thrombosis and Thrombotic Thrombocytopenia Syndrome. Front Neurol. 2021 Nov 22;12:763049. doi: 10.3389/fneur.2021.763049. PMID: 34880826; PMCID: PMC8645635.
10)

Rodriguez EVC, Bouazza FZ, Dauby N, Mullier F, d’Otreppe S, Jissendi Tchofo P, Bartiaux M, Sirjacques C, Roman A, Hermans C, Cliquennois M. Fatal vaccine-induced immune thrombotic thrombocytopenia (VITT) post Ad26.COV2.S: first documented case outside US. Infection. 2022 Apr;50(2):531-536. doi: 10.1007/s15010-021-01712-8. Epub 2021 Oct 9. PMID: 34626338; PMCID: PMC8501343.
11)

Kotal R, Jacob I, Rangappa P, Rao K, Hosurkar G, Anumula SK, Kuberappa AM. A rare case of vaccine-induced immune thrombosis and thrombocytopenia and approach to management. Surg Neurol Int. 2021 Aug 16;12:408. doi: 10.25259/SNI_689_2021. PMID: 34513173; PMCID: PMC8422498.

Delayed cerebral ischemia treatment

Delayed cerebral ischemia treatment

Should We Focus on Blood Pressure or Vasodilatation1)


Rescue treatment for delayed cerebral ischemia (DCI) after subarachnoid hemorrhage can include induced hypertension (iHTN) and, in refractory cases, endovascular approaches, of which selective, continuous intraarterial nimodipine (IAN) is one variant. The combination of iHTN and IAN can dramatically increase vasopressor demand. In case of unsustainable doses, iHTN is often prioritized over IAN. However, evidence in this regard is largely lacking 2)


Level 1 rescue therapy consists of cardiac output optimization, hemoglobin optimization, and endovascular intervention, including angioplasty and intra-arterial vasodilator infusion. In highly refractory cases, level 2 rescue therapies are also considered, none of which have been validated 3).


To date, the only drug shown to be efficacious on both the incidence of vasospasm and poor outcome is nimodipine. Given its modest effects, new pharmacological treatments are being developed to prevent and treat DCI 4)

Volume expansion and hypertension are widely used for the hemodynamic management of patients with subarachnoid hemorrhage to prevent delayed cerebral ischemia.

For small, unruptured, unprotected intracranial aneurysms in SAH patients, the frequency of aneurysm rupture during vasopressor-induced hypertension (VIH) therapy is rare. Reynolds et al. do not recommend withholding VIH therapy from these patients 5).

A randomized pilot trial using a 2-way factorial design allocating patients within 72 hours of subarachnoid hemorrhage to either normovolemia (NV) or volume expansion (HV) and simultaneously to conventional (CBP) or augmented blood pressure (ABP) for 10 days. The study endpoints were protocol adherence and retention to follow-up. The quality of endpoints for a larger trial were 6-month modified Rankin Scale score, comprehensive neurobehavioral assessment, delayed cerebral ischemia, new stroke, and discharge disposition.

This pilot study showed adequate feasibility and excellent retention to follow-up. Given the suggestion of possible worse neurobehavioral outcome with ABP, a larger trial to determine the optimal blood pressure management in this patient population is warranted. (ClinTrials.gov NCT01414894.) 6).

see Delayed cerebral ischemia prevention.


1)

Sadan O, Akbik F. Treating Delayed Cerebral Ischemia: Should We Focus on Blood Pressure or Vasodilatation? Stroke. 2022 Jun 8:101161STROKEAHA122039800. doi: 10.1161/STROKEAHA.122.039800. Epub ahead of print. PMID: 35674047.
2)

Weiss M, Albanna W, Conzen-Dilger C, Kastenholz N, Seyfried K, Ridwan H, Wiesmann M, Veldeman M, Schmidt TP, Megjhani M, Schulze-Steinen H, Clusmann H, Aries MJH, Park S, Schubert GA. Intraarterial Nimodipine Versus Induced Hypertension for Delayed Cerebral Ischemia: A Modified Treatment Protocol. Stroke. 2022 Jun 8:101161STROKEAHA121038216. doi: 10.1161/STROKEAHA.121.038216. Epub ahead of print. PMID: 35674046.
3)

Francoeur CL, Mayer SA. Management of delayed cerebral ischemia after subarachnoid hemorrhage. Crit Care. 2016 Oct 14;20(1):277. doi: 10.1186/s13054-016-1447-6. PMID: 27737684; PMCID: PMC5064957.
4)

Castanares-Zapatero D, Hantson P. Pharmacological treatment of delayed cerebral ischemia and vasospasm in subarachnoid hemorrhage. Ann Intensive Care. 2011 May 24;1(1):12. doi: 10.1186/2110-5820-1-12. PMID: 21906344; PMCID: PMC3224484.
5)

Reynolds MR, Buckley RT, Indrakanti SS, Turkmani AH, Oh G, Crobeddu E, Fargen KM, El Ahmadieh TY, Naidech AM, Amin-Hanjani S, Lanzino G, Hoh BL, Bendok BR, Zipfel GJ. The safety of vasopressor-induced hypertension in subarachnoid hemorrhage patients with coexisting unruptured, unprotected intracranial aneurysms. J Neurosurg. 2015 Oct;123(4):862-71. doi: 10.3171/2014.12.JNS141201. Epub 2015 Jul 24. PubMed PMID: 26207606.
6)

Togashi K, Joffe AM, Sekhar L, Kim L, Lam A, Yanez D, Broeckel-Elrod JA, Moore A, Deem S, Khandelwal N, Souter MJ, Treggiari MM. Randomized Pilot Trial of Intensive Management of Blood Pressure or Volume Expansion in Subarachnoid Hemorrhage (IMPROVES). Neurosurgery. 2015 Feb;76(2):125-35. doi: 10.1227/NEU.0000000000000592. PubMed PMID: 25549192.
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