Surgical Treatment of Intracerebral Hemorrhage

  • Jan Vargas
  • Alejandro M. Spiotta
  • Raymond D. Turner


Spontaneous intracerebral hemorrhage (ICH) is responsible for 10–15% of strokes, with a 1-year mortality rate of more than 40%. Functional independent outcome is estimated at 16.7–24.6% at 1 year following ICH. With the exception of strict blood pressure control, no medical intervention has been shown to improve outcomes for patients with spontaneous ICH. There is a lack of consensus on appropriate treatment despite the theoretical benefits of early hematoma evacuation and prevention of secondary insults following spontaneous ICH. The STITCH trials suggested that while surgery may improve outcomes in some patients with superficial lobar hemorrhages, attempts at targeting deeper lesions may disrupt viable tissue and overcome any benefits yielded by hematoma evacuation. A minimally invasive approach to the evacuation of intracranial hematomas has been a topic of interest for some time. While such approaches to hematoma evacuation have been described for several decades, advances in neuronavigation and neuroimaging have allowed for more precise placement and access of deep-seated lesions, thus minimizing the trauma to viable brain parenchyma and improving success rates. Completion of three ongoing trials (MISTIE-III, INVEST, NICO) will likely change the management of spontaneous ICH in favor of MIS evacuation.


Spontaneous Intracranial hemorrhage Minimally invasive surgery NICO Apollo MISTIE INVEST STITCH Endoscopic hematoma Evacuation 

Spontaneous Intracerebral Hemorrhage

Background and Demographics

Spontaneous intracerebral hemorrhage (ICH) is responsible for 10–15% of strokes, with an annual incidence of 10–30 per 100,000 and a 1-year mortality rate of more than 40% and a 5-year mortality rate of approximately 29.2% [1, 2]. When associated with intraventricular hemorrhage (IVH), the mortality rate increases to 50–80% [3, 4, 5]. Functional independent outcome (defined as an mRS of 0–2) is estimated at 16.7–24.6% at 1 year following ICH [1]. The long-term rate of recurrence is estimated to be 1.3–7.4% per year over an average follow-up of 1–7 years.

ICHs can be divided into supratentorial and infratentorial based on location, with considerable controversy concerning outcomes in patients with primary supratentorial ICH compared to infratentorial ICH.

Craniotomy for Supratentorial Intracranial Hemorrhages

Most ICHs are supratentorial, and spontaneous supratentorial ICH can be further subdivided into deep and superficial. Risk factors for mortality in the setting of ICH are increasing age, decreasing Glasgow Coma Scale score, increasing ICH volume, and presence of intraventricular hemorrhage [1]. The most recent guidelines for the management of spontaneous ICH suggest considering a standard craniotomy for patients with supratentorial lobar hemorrhages within 1 cm of the cortical surface, with the goal being to prevent impending mortality [2].

For patients that do not meet these criteria, there is a lack of consensus on appropriate treatment despite the theoretical benefits of early hematoma evacuation and prevention of secondary insults following spontaneous ICH. The Surgical Trial in Traumatic Intracerebral Hemorrhage (STITCH) trial was a multicenter, randomized investigation that ultimately failed to show any overall benefit to early surgery versus medical management for patients with spontaneous, supratentorial ICH, with favorable outcomes observed in 26% of the surgical group compared to 24% in the medical group [6]. However, a subgroup analysis of the STITCH I data suggested that favorable outcomes were more likely with surgery performed on hematomas less than 1 cm from the cortical surface [7]. These findings lead to the STITCH II trial, which demonstrated similar results and did not show a benefit for the surgical evacuation of superficial lobar hemorrhages [8]. A subsequent meta-analysis of 14 trials of surgery for intracerebral hemorrhage demonstrated improved outcomes with surgery if randomization was performed within 8 h of hemorrhage, if the volume of hematoma was between 20 and 50 mL with a Glasgow Coma Scale of 9–12, or if patient age was between 50 and 69 years [9]. When the results of STITCH II were pooled with this data, the subgroup of patients with lobar intracranial hemorrhage and no IVH demonstrated a trend toward benefit with surgery, but this trend was not significant [8].

The STITCH trials suggested that while surgery may improve outcomes in some patients with superficial lobar hemorrhages, attempts at targeting deeper lesions may disrupt viable tissue and overcome any benefits yielded by hematoma removal. This has led to an interest in developing minimally invasive approaches for accessing and evacuating deep-seated hematomas.

Surgery for Infratentorial Intracranial Hemorrhages

The most recent guidelines for the management of spontaneous ICH published by the American Stroke Association in 2015 recommend immediate surgery for cerebellar hemorrhages with evidence of brainstem compression or hydrocephalus [2]. Despite lack of high-quality evidence, there is data to suggest that suboccipital decompressive craniectomy can reduce mortality when compared to medical therapy alone [10, 11]. These studies advocate for early decompression despite a low GCS in the setting of IVH and fourth ventricular obstruction, on the basis that nonsurgical intervention carries with it a high mortality.

Craniectomy for Spontaneous Intracranial Hemorrhage

The neurological injury caused by spontaneous intracranial hemorrhage is felt to be not only due to the immediate mechanical disruption caused by the original hemorrhage but also from the accumulation of perihematoma edema (PHE) secondary to an inflammatory reaction incited by hemoglobin breakdown products such as iron, and the presence of thrombin. Additionally, there is some evidence that local mass effect limits regional perfusion, causing further secondary ischemic injury. This delayed, second phase of injury results in the extension of damage to potentially viable tissue [5, 12, 13, 14, 15, 16, 17, 18]. As a result, several studies have postulated that the addition of a decompressive craniectomy to hematoma evacuation can decrease ICP and increase cerebral blood perfusion, thus mitigating some of the delayed secondary injury and decreasing the morbidity and mortality [19, 20, 21]. There is limited evidence that hemicraniectomy can improve survival and recovery in patients with aneurysmal and spontaneous intracerebral hemorrhages [22, 23, 24].

A recent prospective controlled trial involving 40 patients with hypertensive ICHs randomized to hematoma evacuation with decompressive craniectomy with expansile duroplasty versus hematoma evacuation only found that adding decompressive craniectomy and duroplasty improved outcomes at 6 months (Fig. 6.1) [25]. In this study, patients with a hematoma volume of at least 60 ml and a GCS of 8 or less were included or if neurological deterioration resulted in surgical evacuation. The authors report that at 6 months, 70% of patients who underwent decompressive craniectomy and expansile duroplasty had a favorable outcome (mRS of 3 or less), compared to 20% in the hematoma-only group, a statistically significant difference. As a result of these data, the most recent American Stroke Association guidelines from 2015 state that craniectomy with or without hematoma evacuation might reduce mortality for patients with supratentorial ICH who are in a coma, have large hematomas with significant midline shift, or have elevated ICP refractory to medical management [2].
Fig. 6.1

Adapted from Moussa and Kheder, 2017. Group A received decompressive craniectomy and expansile duroplasty in addition to hematoma evacuation, whereas Group B only underwent hematoma evacuation. (From Moussa and Khedr [25], with permission of Springer)

Minimally Invasive Surgery for Spontaneous Intracranial Hemorrhage


A minimally invasive approach to the evacuation of intracranial hematomas has been a topic of interest for some time. In 1989, Auer et al. published their experiences in with early endoscopic irrigation and aspiration-based evacuation of ICH. This trial demonstrated a significant improvement in a 6-month mortality rate when compared to medical management [26].

There are several reports of the use of stereotactic minimally invasive techniques such as direct aspiration or mechanical clot disruption to safely remove deeper hemorrhages [26, 27, 28, 29, 30]. More recently, newer methods for hematoma disruption have been introduced, such as ultrasound or injection of recombinant tissue plasminogen activator directly into the hematoma [31, 32].

CLEAR Trials

The Clot Lysis Evaluating Accelerated Resolution of IVH Phase II (CLEAR II) trial aimed to investigate the benefit of clearing intraventricular blood in the setting of spontaneous ICH or subarachnoid hemorrhage [33]. IVH has been shown to be an independent risk factor for poor outcome and occurs in about 40–45% of ICH [7, 34, 35]. The patients who received intraventricular rtPA via an external ventricular drain showed a trend toward lower mortality at 30 days (18% vs. 23% in placebo groups); however this was not statistically significant. There was a significant relationship observed with respect to the rate of clot resolution and clinical improvement at 96 h. In addition, a greater percentage of patients treated with intraventricular tPA demonstrated mRS ≤ 4 (52% vs. 27%) and NIHSS <10 (54% vs. 29%) at 30 days. While the trial was not powered to assess functional outcomes, it demonstrated the safety of a minimally invasive approach to the treatment of IVH and paved the way for the launch of the CLEAR III trial.


The Minimally Invasive Surgery Plus Tissue-Type Plasminogen Activator for ICH Evacuation (MISTIE II) investigation was a controlled, phase II trial which included 123 patients randomized between medical management and minimally invasive surgery followed by catheter drainage with daily rtPA (recombinant tissue plasminogen activator) irrigation. The MISTIE II trial showed a strong trend toward clinical benefit in patients with ICH treated with minimally invasive surgery versus those which received medical management (Fig. 6.2). Surgical patients had a significant reduction in perihematoma edema volume, shorter hospital length of stay and reduced hospital costs, and greater gain activities of daily living scores on the Stroke Impact Scale [31].
Fig. 6.2

The results of the MISTIE trial suggested improved outcomes and shorted hospital stay following minimally invasive catheter placement. Modified ranking shift at 1 year

New Techniques for MIS Evacuations


The Penumbra Apollo (Penumbra Inc., Alameda CA) is an aspiration-irrigation system which allows the removal of hemorrhage via a wand with controlled aspiration. A vibrational element housed within the wand vibrates at high frequency to break down the hemorrhagic products inside of the wand and prevent clogging. The wand can be used in conjunction with commercially available endoscopes and is positioned in the hematoma under stereotactic guidance via a cranial burr hole with a small dural incision (Figs. 6.3, 6.4, 6.5, 6.6, and 6.7). Since its approval, the Apollo system has been used for the evacuation of both intraventricular and intracerebral hemorrhages, including those associated with ruptured aneurysms [36, 37, 38, 39].
Fig. 6.3

(a) Apollo wand. (With permission of Penumbra, Inc.), (b) Apollo system. (With permission of Penumbra, Inc.)

Fig. 6.4

Setup with endoscope

Fig. 6.5

Endoscopic view of hematoma and/or ICH evac cavity

Fig. 6.6

(a, b) Pre-Apollo evac examples

Fig. 6.7

(a, b) Post-Apollo evac samples


The NICO BrainPath system consists of a 13.5 mm sheath with an internal obturator that is placed stereotactically through a small craniotomy into intracranial hematomas. The obturator is designed to displace rather than disrupt brain parenchyma during placement, minimizing damage to underlying functional tissue. Once placed, the obturator is removed, allowing access to the hematoma which can be evacuated using conventional suction and bipolar cautery under the operating microscope or an exoscope which is aligned down the length of the BrainPath sheath. The NICO BrainPath sheath has been approved for visualization of the surgical field during brain and spinal surgery.

In addition to its BrainPath sheath, NICO also manufactures the Myriad handpiece, consisting of a wand with a side port equipped with a reciprocating cutting blade. The handpiece has an aspiration mechanism that pulls tissue into the side port. Using a foot pedal, the surgeon can both control the strength of aspiration and turn the cutting blade on or off. The Myriad handpiece has been approved for the morcellation and removal of tissue during pelviscopic, laparoscopic, percutaneous, and open surgical procedures whenever access to the surgical site is limited.

The NICO BrainPath has been successfully used for the evacuation of intracerebral hematomas, with reported at least 87% reduction in hematoma volume, although 3 of the 11 patients (27%) suffered postoperative complications including a fatal hemorrhage [40, 41] (Fig. 6.8).
Fig. 6.8

(ICH pre and post MIS evacuation). (a) Large right ICH hemorrhage approaching the cortical surface. (b) Post-NICO evacuation of the hemorrhage

Upcoming Trials

The encouraging findings of recent case series have led to the development of several randomized controlled trials to investigate MIS techniques.

Minimally Invasive Endoscopic Surgical Treatment with Apollo Versus Medical Management for Supratentorial ICH (INVEST) trial is a phase II trial which will compare ICH evacuation using the Apollo system to medical management in 222 patients with moderate to large (30–80 cm3) spontaneous supratentorial hemorrhages [42]. The NICO BrainPath system will also be part of a randomized controlled trial, which will include up to 10 centers.

Timing of Surgery

The current American Stroke Association guidelines from 2015 do not have any recommendations regarding early evacuation versus waiting for a neurological decline, reflecting the significant controversy regarding the timing of surgery for spontaneous intracranial hemorrhage [2]. However, there is data suggesting that approximately 50% of deaths from spontaneous ICH occur within the first 48 h [43]. Although the STITCH I trial failed to demonstrate added benefit for early surgery, a subgroup analysis of STITCH II demonstrated that there may be a benefit of surgery if performed before 21 h of ictus [8]. Additionally, there is data suggesting that surgery within the first 12–24 h improves neurologic function [44, 45]. A meta-analysis performed by Gregson et al. suggested that operation on supratentorial spontaneous ICH within 8 h of ictus was beneficial with an OR of 0.59 [9].

Despite the lack of evidence, currently guidelines suggest that supratentorial hematoma evacuation in deteriorating patients might be considered as a life-saving measure [37].


  1. 1.
    Poon MT, Fonville AF, Al-Shahi Salman R. Long-term prognosis after intracerebral haemorrhage: systematic review and meta-analysis. J Neurol Neurosurg Psychiatry. 2014;85(6):660–7.CrossRefPubMedGoogle Scholar
  2. 2.
    Hemphill JC 3rd, Greenberg SM, Anderson CS, Becker K, Bendok BR, Cushman M, et al. Guidelines for the management of spontaneous intracerebral hemorrhage: a guideline for healthcare professionals from the American Heart Association/American Stroke Association. Stroke. 2015;46(7):2032–60.CrossRefPubMedGoogle Scholar
  3. 3.
    Dennis MS. Outcome after brain haemorrhage. Cerebrovasc Dis. 2003;16(Suppl 1):9–13.CrossRefPubMedGoogle Scholar
  4. 4.
    Labovitz DL, Halim A, Boden-Albala B, Hauser WA, Sacco RL. The incidence of deep and lobar intracerebral hemorrhage in whites, blacks, and Hispanics. Neurology. 2005;65(4):518–22.CrossRefPubMedGoogle Scholar
  5. 5.
    Qureshi AI, Mendelow AD, Hanley DF. Intracerebral haemorrhage. Lancet. 2009;373(9675):1632–44.CrossRefPubMedPubMedCentralGoogle Scholar
  6. 6.
    Mendelow AD, Gregson BA, Fernandes HM, Murray GD, Teasdale GM, Hope DT, et al. Early surgery versus initial conservative treatment in patients with spontaneous supratentorial intracerebral haematomas in the International Surgical Trial in Intracerebral Haemorrhage (STICH): a randomised trial. Lancet. 2005;365(9457):387–97.CrossRefPubMedGoogle Scholar
  7. 7.
    Bhattathiri PS, Gregson B, Prasad KS, Mendelow AD, Investigators S. Intraventricular hemorrhage and hydrocephalus after spontaneous intracerebral hemorrhage: results from the STICH trial. Acta Neurochir Suppl. 2006;96:65–8.CrossRefPubMedGoogle Scholar
  8. 8.
    Mendelow AD, Gregson BA, Rowan EN, Murray GD, Gholkar A, Mitchell PM, et al. Early surgery versus initial conservative treatment in patients with spontaneous supratentorial lobar intracerebral haematomas (STICH II): a randomised trial. Lancet. 2013;382(9890):397–408.CrossRefPubMedPubMedCentralGoogle Scholar
  9. 9.
    Gregson BA, Broderick JP, Auer LM, Batjer H, Chen XC, Juvela S, et al. Individual patient data subgroup meta-analysis of surgery for spontaneous supratentorial intracerebral hemorrhage. Stroke. 2012;43(6):1496–504.CrossRefPubMedPubMedCentralGoogle Scholar
  10. 10.
    Luney MS, English SW, Longworth A, Simpson J, Gudibande S, Matta B, et al. Acute posterior cranial fossa hemorrhage-is surgical decompression better than expectant medical management? Neurocrit Care. 2016;25(3):365–70.CrossRefPubMedPubMedCentralGoogle Scholar
  11. 11.
    Kirollos RW, Tyagi AK, Ross SA, van Hille PT, Marks PV. Management of spontaneous cerebellar hematomas: a prospective treatment protocol. Neurosurgery. 2001;49(6):1378–86; discussion 86-7CrossRefPubMedGoogle Scholar
  12. 12.
    Xi G, Wagner KR, Keep RF, Hua Y, de Courten-Myers GM, Broderick JP, et al. Role of blood clot formation on early edema development after experimental intracerebral hemorrhage. Stroke. 1998;29(12):2580–6.CrossRefPubMedGoogle Scholar
  13. 13.
    Lee KR, Kawai N, Kim S, Sagher O, Hoff JT. Mechanisms of edema formation after intracerebral hemorrhage: effects of thrombin on cerebral blood flow, blood-brain barrier permeability, and cell survival in a rat model. J Neurosurg. 1997;86(2):272–8.CrossRefPubMedGoogle Scholar
  14. 14.
    Lee KR, Colon GP, Betz AL, Keep RF, Kim S, Hoff JT. Edema from intracerebral hemorrhage: the role of thrombin. J Neurosurg. 1996;84(1):91–6.CrossRefPubMedGoogle Scholar
  15. 15.
    Wang G, Shao A, Hu W, Xue F, Zhao H, Jin X, et al. Changes of ferrous iron and its transporters after intracerebral hemorrhage in rats. Int J Clin Exp Pathol. 2015;8(9):10671–9.PubMedPubMedCentralGoogle Scholar
  16. 16.
    Wang G, Hu W, Tang Q, Wang L, Sun XG, Chen Y, et al. Effect comparison of both iron chelators on outcomes, iron deposit, and iron transporters after intracerebral hemorrhage in rats. Mol Neurobiol. 2016;53(6):3576–85.CrossRefPubMedGoogle Scholar
  17. 17.
    Qing WG, Dong YQ, Ping TQ, Lai LG, Fang LD, Min HW, et al. Brain edema after intracerebral hemorrhage in rats: the role of iron overload and aquaporin 4. J Neurosurg. 2009;110(3):462–8.CrossRefPubMedGoogle Scholar
  18. 18.
    Xi G, Keep RF, Hoff JT. Erythrocytes and delayed brain edema formation following intracerebral hemorrhage in rats. J Neurosurg. 1998;89(6):991–6.CrossRefPubMedGoogle Scholar
  19. 19.
    Diringer MN, Edwards DF, Zazulia AR. Hydrocephalus: a previously unrecognized predictor of poor outcome from supratentorial intracerebral hemorrhage. Stroke. 1998;29(7):1352–7.CrossRefPubMedGoogle Scholar
  20. 20.
    Gebel JM Jr, Jauch EC, Brott TG, Khoury J, Sauerbeck L, Salisbury S, et al. Natural history of perihematomal edema in patients with hyperacute spontaneous intracerebral hemorrhage. Stroke. 2002;33(11):2631–5.CrossRefPubMedGoogle Scholar
  21. 21.
    Xi G, Fewel ME, Hua Y, Thompson BG Jr, Hoff JT, Keep RF. Intracerebral hemorrhage: pathophysiology and therapy. Neurocrit Care. 2004;1(1):5–18.CrossRefPubMedGoogle Scholar
  22. 22.
    Schirmer CM, Hoit DA, Malek AM. Decompressive hemicraniectomy for the treatment of intractable intracranial hypertension after aneurysmal subarachnoid hemorrhage. Stroke. 2007;38(3):987–92.CrossRefPubMedGoogle Scholar
  23. 23.
    Dierssen G, Carda R, Coca JM. The influence of large decompressive craniectomy on the outcome of surgical treatment in spontaneous intracerebral haematomas. Acta Neurochir. 1983;69(1–2):53–60.CrossRefPubMedGoogle Scholar
  24. 24.
    Ziai WC, Port JD, Cowan JA, Garonzik IM, Bhardwaj A, Rigamonti D. Decompressive craniectomy for intractable cerebral edema: experience of a single center. J Neurosurg Anesthesiol. 2003;15(1):25–32.CrossRefPubMedGoogle Scholar
  25. 25.
    Moussa WM, Khedr W. Decompressive craniectomy and expansive duraplasty with evacuation of hypertensive intracerebral hematoma, a randomized controlled trial. Neurosurg Rev. 2017;40(1):115–27.CrossRefPubMedGoogle Scholar
  26. 26.
    Auer LM, Deinsberger W, Niederkorn K, Gell G, Kleinert R, Schneider G, et al. Endoscopic surgery versus medical treatment for spontaneous intracerebral hematoma: a randomized study. J Neurosurg. 1989;70(4):530–5.CrossRefPubMedGoogle Scholar
  27. 27.
    Backlund EO, von Holst H. Controlled subtotal evacuation of intracerebral haematomas by stereotactic technique. Surg Neurol. 1978;9(2):99–101.PubMedGoogle Scholar
  28. 28.
    Barrett RJ, Hussain R, Coplin WM, Berry S, Keyl PM, Hanley DF, et al. Frameless stereotactic aspiration and thrombolysis of spontaneous intracerebral hemorrhage. Neurocrit Care. 2005;3(3):237–45.CrossRefPubMedGoogle Scholar
  29. 29.
    Higgins AC, Nashold BS, Cosman E. Stereotactic evacuation of primary intracerebral hematomas: new instrumentation. Appl Neurophysiol. 1982;45(4–5):438–42.PubMedGoogle Scholar
  30. 30.
    Marquardt G, Wolff R, Janzen RW, Seifert V. Basal ganglia haematomas in non-comatose patients: subacute stereotactic aspiration improves long-term outcome in comparison to purely medical treatment. Neurosurg Rev. 2005;28(1):64–9.PubMedGoogle Scholar
  31. 31.
    Mould WA, Carhuapoma JR, Muschelli J, Lane K, Morgan TC, McBee NA, et al. Minimally invasive surgery plus recombinant tissue-type plasminogen activator for intracerebral hemorrhage evacuation decreases perihematomal edema. Stroke. 2013;44(3):627–34.CrossRefPubMedPubMedCentralGoogle Scholar
  32. 32.
    Newell DW, Shah MM, Wilcox R, Hansmann DR, Melnychuk E, Muschelli J, et al. Minimally invasive evacuation of spontaneous intracerebral hemorrhage using sonothrombolysis. J Neurosurg. 2011;115(3):592–601.CrossRefPubMedPubMedCentralGoogle Scholar
  33. 33.
    Naff N, Williams MA, Keyl PM, Tuhrim S, Bullock MR, Mayer SA, et al. Low-dose recombinant tissue-type plasminogen activator enhances clot resolution in brain hemorrhage: the intraventricular hemorrhage thrombolysis trial. Stroke. 2011;42(11):3009–16.CrossRefPubMedPubMedCentralGoogle Scholar
  34. 34.
    Daverat P, Castel JP, Dartigues JF, Orgogozo JM. Death and functional outcome after spontaneous intracerebral hemorrhage. A prospective study of 166 cases using multivariate analysis. Stroke. 1991;22(1):1–6.CrossRefPubMedGoogle Scholar
  35. 35.
    Hallevi H, Albright KC, Aronowski J, Barreto AD, Martin-Schild S, Khaja AM, et al. Intraventricular hemorrhage: anatomic relationships and clinical implications. Neurology. 2008;70(11):848–52.CrossRefPubMedPubMedCentralGoogle Scholar
  36. 36.
    Fiorella D, Gutman F, Woo H, Arthur A, Aranguren R, Davis R. Minimally invasive evacuation of parenchymal and ventricular hemorrhage using the Apollo system with simultaneous neuronavigation, neuroendoscopy and active monitoring with cone beam CT. J Neurointerv Surg. 2015;7(10):752–7.CrossRefPubMedGoogle Scholar
  37. 37.
    Spiotta AM, Fiorella D, Vargas J, Khalessi A, Hoit D, Arthur A, et al. Initial multicenter technical experience with the Apollo device for minimally invasive intracerebral hematoma evacuation. Neurosurgery. 2015;11(Suppl 2):243–51; discussion 51.CrossRefPubMedGoogle Scholar
  38. 38.
    Tan LA, Lopes DK, Munoz LF, Shah Y, Bhabad S, Jhaveri M, et al. Minimally invasive evacuation of intraventricular hemorrhage with the Apollo vibration/suction device. J Clin Neurosci Off J Neurosurg Soc Australas. 2016;27:53–8.Google Scholar
  39. 39.
    Turner RD, Vargas J, Turk AS, Chaudry MI, Spiotta AM. Novel device and technique for minimally invasive intracerebral hematoma evacuation in the same setting of a ruptured intracranial aneurysm: combined treatment in the neurointerventional angiography suite. Neurosurgery. 2015;11(Suppl 2):43–50; discussion -1.PubMedGoogle Scholar
  40. 40.
    Ding D, Przybylowski CJ, Starke RM, Sterling Street R, Tyree AE, Webster Crowley R, et al. A minimally invasive anterior skull base approach for evacuation of a basal ganglia hemorrhage. J Clin Neurosci Off J Neurosurg Soc Australas. 2015;22(11):1816–9.Google Scholar
  41. 41.
    Przybylowski CJ, Ding D, Starke RM, Webster Crowley R, Liu KC. Endoport-assisted surgery for the management of spontaneous intracerebral hemorrhage. J Clin Neurosci Off J Neurosurg Soc Australas. 2015;22(11):1727–32.Google Scholar
  42. 42.
    Fiorella D, Arthur AS, Mocco JD. 305 The INVEST trial: a randomized, controlled trial to investigate the safety and efficacy of image-guided minimally invasive endoscopic surgery with Apollo vs best medical management for supratentorial intracerebral hemorrhage. Neurosurgery. 2016;63(Suppl 1):187.CrossRefGoogle Scholar
  43. 43.
    Broderick JP, Brott TG, Duldner JE, Tomsick T, Huster G. Volume of intracerebral hemorrhage. A powerful and easy-to-use predictor of 30-day mortality. Stroke. 1993;24(7):987–93.CrossRefPubMedGoogle Scholar
  44. 44.
    Wang YF, Wu JS, Mao Y, Chen XC, Zhou LF, Zhang Y. The optimal time-window for surgical treatment of spontaneous intracerebral hemorrhage: result of prospective randomized controlled trial of 500 cases. Acta Neurochir Suppl. 2008;105:141–5.CrossRefPubMedGoogle Scholar
  45. 45.
    Maila SK. Factors affecting the outcome of surgical evacuation of spontaneous deep intra cerebral bleeds. Br J Neurosurg. 2015;29(5):668–71.CrossRefPubMedGoogle Scholar

Copyright information

© Springer International Publishing AG, part of Springer Nature 2018

Authors and Affiliations

  • Jan Vargas
    • 1
  • Alejandro M. Spiotta
    • 1
  • Raymond D. Turner
    • 1
  1. 1.Department of Neurosurgery, Medical University of South CarolinaCharlestonUSA

Personalised recommendations