REVIEW URRENT C OPINION

Malignant middle cerebral artery infarction Katja E. Wartenberg

Purpose of review This review will report on the new aspects of management of ‘malignant’ middle cerebral artery (MCA) infarctions. Recent findings Large MCA infarctions have been associated with high death rates for years. The most reliable predictors of a ‘malignant’ course are hypodensity in more than 50% of the MCA territory on computed tomography as well as stroke volume greater than 145 ml on diffusion-weighted imaging. Real-time neuromonitoring may be helpful in the detection of development of cerebral edema. The attempt of recanalization of the affected artery utilizing a combination of intravenous and intra-arterial thrombolysis and mechanical thrombectomy is crucial. Monitoring of intracranial pressure has not been proven helpful. Decompressive surgery within 48 h after symptom onset in patients less than 60 years old reduces mortality and severe disability. The quality of life perceived by the survivors is variable and deserves further study. The neuroprotective effect of hypothermia requires additional investigation. Summary The era of decompressive hemicraniectomy has changed the prospects of patients with large infarctions in the MCA or internal carotid artery territory who are at risk of development of ‘malignant’ cerebral edema. Timing of surgery and appropriate patient selection based on age and other criteria need to be refined. Keywords cerebral edema, decompression, hemicraniectomy, malignant MCA infarction, malignant stroke

INTRODUCTION Large hemispheric infarctions because of middle cerebral artery (MCA) or internal carotid artery (ICA) occlusion constitute a major cause of severe morbidity and mortality. Neurological deterioration occurs as a consequence of space-occupying cerebral edema in approximately 10% of all hemispheric strokes and 5% of all ischemic strokes which led to the term ‘malignant MCA infarction’ [1–3]. Mortality ranges between 41 and 79% with conservative treatment in the intensive care unit [1–5]. However, the new era of decompressive craniectomy resulted in a dramatic decrease of mortality and severe disability [6–9]. The patients affected are generally 10 years younger (56
9.4 years) than the average stroke patient [1]. The incidence ranges between 10 and 20 per 100 000 per year [1]. Large hemispheric infarctions occur as a consequence of a thrombotic or embolic occlusion of the distal ICA or the proximal MCA trunk without sufficient collateral flow (Figs 1 and 2). Depending on the presence of sufficient collaterals, mainly leptomeningeal arteries, or anatomic variants, the www.co-criticalcare.com

infarction may include the anterior and/or posterior territory as well [10,11]. Most patients have risk factors for vascular disease such as hypertension, diabetes, hypercholesteremia, tobacco abuse, history of transient ischemic attacks or ischemic strokes, congestive heart failure, and coronary artery disease. Atrial fibrillation is more frequent in patients with MCA and ICA territory strokes compared to the remaining stroke population [1–3,12]. ICA dissection is a significant cause of large territory infarctions in younger patients (12%) [12]. The patients present with hemiparesis, hemiplegia, hemisensory loss, homonymous hemianopia contralateral to the site of infarction, partial and Neurointensive Care Unit, Martin-Luther-University, Halle-Wittenberg, Halle, Germany Correspondence to Katja E. Wartenberg, MD, PhD, Neurointensive Care Unit, Martin-Luther-University, Halle-Wittenberg, Ernst-Grube-Strasse 40, 06120 Halle, Germany. Tel: +49 345 557 2934; fax: +49 345 557 2935; e-mail: [email protected] Curr Opin Crit Care 2012, 18:152–163 DOI:10.1097/MCC.0b013e32835075c5 Volume 18  Number 2  April 2012

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Malignant middle cerebral artery infarction Wartenberg

KEY POINTS  The most reliable predictors of a ‘malignant’ course of large hemispheric strokes are infarction of more than 50% of the MCA territory and a perfusion deficit of more than 66% on CT as well as stroke volume in diffusion-weighted imaging of greater than 145 ml within 14 h and greater than 82 ml within 6 h of symptom onset.  Close neuromonitoring with continuous EEG, intracortical electrodes, microdialysis, and brain tissue oxygenation may be helpful in early detection of development of cerebral edema.  Recanalization of the affected artery utilizing a combination of intravenous and intra-arterial thrombolysis and/or mechanical thrombectomy within 3–6 h, as early as possible, should be attempted.  Monitoring of intracranial pressure has not been proven helpful. ICP can be normal in the setting of herniation.  Decompressive surgery within 48 h after symptom onset in patients less than 60 years old reduces mortality, moderate (mRS 3) and severe disability (mRS 4). The number needed to treat (NNT) for survival and severe disability is 2, the NNT for moderate disability equals 6.

fixed gaze palsy towards the nonaffected hemisphere, and depressed level of awareness. Nondominant hemispheric infarctions are associated with visual, motor, and sensory neglect. Language disturbance such as fluent, nonfluent, and mostly global aphasia are typical for infarctions localized to the dominant hemisphere [1,12]. Neurological decline starts mostly within the first 48 h [1,3], in 36% within 24 h, and 68% within 48 h [3]. Clinical signs for development of cerebral

FIGURE 1. Magnetic resonance angiogram time-of-flight image showing distal occlusion of the left internal carotid artery (carotid T occlusion).

FIGURE 2. Cerebral angiography with right internal carotid injection showing occlusion of the M1 segment of the right middle cerebral artery.

edema include nausea and emesis, decreasing level of consciousness to coma, increasing pupillary size ipsilateral to the infarct, hemiparesis ipsilateral to the infarct, unilateral or bilateral flexor or extensor posturing, altered breathing pattern, respiratory failure, bradycardia, and hypertension (Cushing response) [1,3,4]. The first sign is drowsiness followed by pupillary asymmetry, periodic breathing, and extensor plantar response ipsilateral to the site of infarction [13]. Death occurs within 5 days [1,3,4] as a result of brain death in the majority of patients, cardiac arrhythmias and arrest, sepsis, recurrent stroke, and pneumonia [1–3]. Hemispheric brain swelling leads to brain tissue shifts with subsequent brain stem distortion, bihemispheric dysfunction through mechanical displacement, vascular compression, uncal and transtentorial herniation. The global intracranial pressure (ICP) is usually not elevated in large

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Neuroscience

hemispheric infarctions; cerebral hypoperfusion is not the cause for early neurological deterioration brain death [1,14,15 ]. &

PREDICTORS OF MALIGNANT MIDDLE CEREBRAL ARTERY INFARCTION With increasing availability of decompressive craniectomy as an aggressive treatment option, identification of predictors of a malignant course of the MCA or ICA infarction is exceedingly important. Several clinical and radiological predictors of development of brain swelling and poor outcome are summarized in Table 1 [2,11,16–40]. The metaanalysis by Hofmeijer et al. [41] included 23 studies and found involvement of more than 50% of the MCA territory (Fig. 3) and a perfusion deficit of more than 66% on computed tomography (CT) to be the most reliable predictors of edema formation. Other associated predictors with moderate effect size were early mass effect, involvement of other vascular territories, higher body temperature, ICA occlusion, and mechanical ventilation. A head CT showing ischemic infarction of more than twothirds of the MCA territory with either involvement of the basal ganglia or evidence of developing cerebral edema was also chosen as inclusion criterion in two randomized hemicraniectomy trials [6,7]. Utilizing magnetic resonance tomography with diffusion-weighted imaging (DWI), stroke volumes of greater than 145 ml within 14 h of symptom onset [19] and of greater than 82 ml within 6 h [27] were found to be reliable predictors of a malignant course. More recently, multimodality monitoring including brain tissue oxygenation, cerebral metabolites by microdialysis, continuous and intracortical electroencephalography (EEG) revealed new insights into the development of malignant brain edema [38–40,42,43]. An increase in periinfarct extracellular glutamate, glycerin, and lactate concentration, and an augmentation of the lactate/ pyruvate ratio was thought to reflect developing brain edema with subsequent secondary neuronal ischemia, as those changes of neurochemicals preceded an increase in ICP [39,43]. Impaired autoregulation, decreased brain tissue oxygenation, and low cerebral perfusion pressure (CPP) were shown surrounding the infarct [38,40]. Bosche et al. [42] found significantly lower nontransmitter amino acid concentrations in the areas adjacent to the infarct in patients who developed malignant brain edema. The presence of a peak of faster EEG activity (5–7 Hz) in EEG power spectra obtained from continuous EEG monitoring after hemicraniectomy was correlated with an improved level of consciousness 154

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&

and functional outcome at discharge [44 ]. Cortical spreading depression and peri-infarct depolarizations were seen on cortical EEG strips inserted during hemicraniectomy procedures in all patients with electrodes placed correctly in areas adjacent to infarcted tissue. The time for the EEG to recover was longer after clusters of cortical-spreading depressions indicating progressive deterioration of the metabolic or hemodynamic status in peri-infarct tissue [45].

MANAGEMENT OF ACUTE ISCHEMIC INFARCTION Successful recanalization of the hypoperfused or occluded MCA or ICA within a narrow time window of 3–4.5 h can be lifesaving and decrease the size of infarction, thereby preventing the development of malignant brain edema [46–49]. Intravenous recombinant tissue plasminogen activator (rtPA) administered within 3 h of onset of the first stroke symptom is the only approved acute stroke treatment [46,49,50]. Extension of the time window up to 4.5 h has been demonstrated to be safe and efficacious [48]. However, intravenous thrombolysis is less likely to reperfuse large cerebral artery occlusions such as in ‘malignant’ MCA infarctions [51 ]. The PROACT trials investigated safety and feasibility of intra-arterially administered recombinant prourokinase within 6 h of stroke onset. The recanalization rate was 66% with a 10% risk of intracerebral hemorrhage [52,53]. A meta-analysis including 395 patients from five trials showed a rate of partial or complete vessel recanalization of 46.8% with intra-arterial fibrinolysis with 14.8% good and 13.0% excellent outcomes. The discrepancy between recanalization rates and outcomes may be explained by prolonged times from stroke onset to procedure [54]. In the meantime, several devices for mechanical recanalization have become available: the Mechanical Embolus Removal in Cerebral Ischemia (MERCI; Concentric Medical, Inc., Mountainview, California, USA, see Fig. 4), a corkscrewshaped device to pull the thrombus into an extracranial guide catheter under active suction; the Penumbra stroke system (Penumbra, Inc., Alameda, California, USA) for clot aspiration and extraction with catheter position proximal to the occlusion; Solitaire (Covidien/eV3, Maple Grove, Minnesota, USA), or Trevo (Concentric Medical, Inc., Mountainview, California, USA) which are combined removable stent and clot retriever devices [51 ]. None of these devices have been evaluated in a randomized controlled trial regarding their effect on long-term outcome. Acute stenting and angioplasty of intracranial stenosis with the Wingspan stent &

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Malignant middle cerebral artery infarction Wartenberg Table 1. Clinical and radiological predictors of a malignant course of infarctions in the middle cerebral or internal carotid artery territories Predictor

Number of patients

Odds ratio or sensitivity/specificity

Study

Demographic and clinical predictors Younger age

192

OR 0.4, 95% CI 0.3–0.6, P < 0.0001

Jaramillo et al., Neurology 2006 [11]

Female sex

192 24

OR 8.2, 95% CI 2.7–25.2, P ¼ 0.0003 72 vs. 20%

Jaramillo et al., Neurology, 2006 [11] Maramattom et al., Neurology 2004 [16] Jaramillo et al., Neurology 2006 [11]

No previous ischemic infarctions

192

OR 0.2, 95% CI 0.05–0.7, P ¼ 0.01

12 h systolic BP 180 mmHg

135

OR 4.2, 95% CI 1.4–12.9, P ¼ 0.01

Krieger et al., Stroke 1999 [17]

History of hypertension

201

OR 3.0, 95% CI 1.2–7.6, P ¼ 0.02

Kasner et al., Stroke 2001 [2] Kasner et al., Stroke 2001 [2]

History of congestive heart failure

201

OR 2.1, 95% CI 1.5–3.0, P ¼ 0.001

Coronary artery disease

62

OR 8.5, 95% CI 1.4–50.8, P ¼ 0.02

Wang et al., Eur J Neurology 2006 [18]

High white blood cell count

201

OR 1.08 per 1000 white blood cells/ml, 95% CI 1.01–1.14, P ¼ 0.02

Kasner et al., Stroke 2001 [2]

Severe clinical deficit on admission NIHSS >20

28

100% sensitivity, 78% specificity

Oppenheim et al., Stroke 2000 [19]

NIHSS 19

37

96% sensitivity, 72% specificity

Thomalla et al., Stroke 2003 [20]

Total Glasgow Coma Scale score

62

OR 0.6, 95% CI 0.4–0.9, P ¼ 0.006

Wang et al., Eur J Neurology 2006 [18]

Nausea and vomiting within 24 h

135

OR 5.1, 95% CI 1.7–15.3, P ¼ 0.003

Krieger et al., Stroke 1999 [17]

Protein S-100 >0.35 mg/l at 12 h >1.03 mg/l at 24 h

51

Cellular fibronectin 16.6 mg/ml Matrix metalloproteinase 9 140 ng/ml

40

90% sensitivity, 100% specificity 64% sensitivity, 88% specificity

Serena et al., Stroke 2005 [22]

Hypodensity in MCA territory on initial CT >50%

135 201 36

OR 6.1, 95% CI 2.3–16.6, P ¼ 0.0004 OR 6.3, 95% CI 3.5–11.6, P ¼ 0.001 OR 14.0, 95% CI 1.04–189.4, P ¼ 0.047

Krieger et al., Stroke 1999 [17] Kasner et al., Stroke 2001 [2] Manno et al., Mayo Clin Proc 2003 [23]

Horizontal pineal displacement >4 mm on CT within 48 h of stroke onset

127

46% sensitivity, 89% specificity

Pullicino et al., Neurology 1997 [24]

Attenuation of the lentiform nucleus, loss of the insular ribbon, or hemispheric sulcal effacement

100

Internal carotid T occlusion

74 37

Foerch et al., Stroke 2004 [21] 75% sensitivity, 80% specificity 94% sensitivity, 83% specificity

Radiological predictors – computed tomography

Moulin et al., Neurology 1996 [25]

OR 5.3, 95% CI 1.7–16.2, P ¼ 0.01 64% sensitivity, 85% specificity

Kucinski et al., AJNR 1998 [26] Thomalla et al., Stroke 2003 [20]

Combined ICA and MCA occlusion

140

OR 5.4, 95% CI 1.6–18.7, P ¼ 0.008

Thomalla et al., Ann Neurol 2010 [27]

Involvement of additional vascular territories (ACA, PCA, anterior choroidal)

201 24

OR 3.3, 95% CI 1.2–9.4, P ¼ 0.02 72 vs. 0%

Kasner et al., Stroke 2001 [2] Maramattom et al., Neurology 2004 [16]

Hyperdense MCA sign

62 36

71% sensitivity, 84% specificity OR 21.6, 95% CI 3.5–130.0, P < 0.001

Haring et al., Stroke 1999 [28] Manno et al., Mayo Clin Proc 2003 [23]

Attenuated corticomedullary contrast within 18 h of symptom onset

62

87% sensitivity, 97% specificity

Haring et al., Stroke 1999 [28]

Perfusion deficit >50% of MCA territory on CT within 6 h of stroke onset

31

Perfusion deficit >66% of MCA territory on CT within 6 h of stroke onset

27

91% sensitivity, 94% specificity

Ryoo et al., J Comput Assist Tomogr 2004 [30]

Infarction core on cerebral blood flow maps >27.9%

106

85% sensitivity, 78% specificity

Dittrich et al., J Neurol 2008 [31]

Lee et al., Arch Neurol 2004 [29]

Cerebral blood volume maps >22.8%

85% sensitivity, 74% specificity

Time to peak maps >39.9% of the hemisphere on perfusion CT (median 2 h after stroke onset)

95% sensitivity, 72% specificity

Increased infarct permeability area on perfusion CT on average within 6 h after symptom onset

122

Cerebral blood volume to cerebrospinal fluid volume ratio >0.92 on perfusion CT within 6 h after symptom onset

52

Single-photon emission CT flow deficit

26

Bektas et al., Stroke 2010 [32]

96% sensitivity, 96% specificity

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Minnerup et al., Stroke 2011 [33]

Limburg et al., Stroke 1990 [34]

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Neuroscience Table 1 (Continued) Number of patients

Predictor

Odds ratio or sensitivity/specificity

Study

Xenon-enhanced CT within 6 h of stroke onset

20

Mean CBF 8.6 ml/100 g/min correlated with herniation

Firlik et al., J Neurosurg 1998 [35]

99mTc-ECD SPECT deficit in the entire MCA territory within 6 h of stroke onset

108

82% sensitivity, 99% specificity

Berrouschot et al., Stroke 1998 [36]

99mTc-DTPA SPECT DTPA disruption index within 36 h after stroke onset

25

Significant correlation with herniation

Lampl et al., Brain Res 2006 [37]

Radiological predictors – magnetic resonance imaging DWI volume >145 ml within 14 h of stroke onset

28

100% sensitivity, 94% specificity

Oppenheim et al., Stroke 2000 [19]

ADC82 ml within 6 h of stroke onset

37

87% sensitivity, 91% specificity

Thomalla et al., Stroke 2003 [20]

DWI volume >82 ml within 6 h of symptom onset

140

52% sensitivity, 98% specificity

Thomalla et al., Ann Neurol 2010 [27]

TTP lesion volume >162 ml

37

83% sensitivity, 75% specificity

Thomalla et al., Stroke 2003 [20]

34

99% sensitivity, 86% specificity

Dohmen et al., Stroke 2003 [38]

Other radiological predictors PET mean cerebral blood flow in infarction core 82 ml on ADC or DWI within 6 h). Further investigation of multimodality monitoring with probes inserted adjacent to the infarct may refine the selection of patients who develop cerebral edema. Hypothermia is a promising additional tool for control of cerebral edema with a beneficial neuroprotective effect that requires further investigation. Acknowledgements None. Conflicts of interest The author has no conflicts of interest and no financial support to disclose.

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Malignant middle cerebral artery infarction Wartenberg 59. Diringer MN, Scalfani MT, Zazulia AR, et al. Cerebral hemodynamic and metabolic effects of equi-osmolar doses mannitol and 23.4% saline in patients with edema following large ischemic stroke. Neurocrit Care 2011; 14:11–17. 60. Schwarz S, Schwab S, Bertram M, et al. Effects of hypertonic saline hydroxyethyl starch solution and mannitol in patients with increased intracranial pressure after stroke. Stroke 1998; 29:1550–1555. 61. Kamel H, Navi BB, Nakagawa K, et al. Hypertonic saline versus mannitol for & the treatment of elevated intracranial pressure: a meta-analysis of randomized clinical trials. Crit Care Med 2011; 39:554–559. This is an interesting comparison of the effects of mannitol and hypertonic saline on intracranial hypertension in absence of a randomized trial. 62. Hays AN, Lazaridis C, Neyens R, et al. Osmotherapy: use among neurointensivists. Neurocrit Care 2011; 14:222–228. 63. Van der Worp HB, Sena ES, Donnan GA, et al. Hypothermia in animal models of acute ischaemic stroke: a systematic review and meta-analysis. Brain 2007; 130 (Pt 12):3063–3074. 64. Schwab S, Schwarz S, Spranger M, et al. Moderate hypothermia in the treatment of patients with severe middle cerebral artery infarction. Stroke 1998; 29:2461–2466. 65. Steiner T, Friede T, Aschoff A, et al. Effect and feasibility of controlled rewarming after moderate hypothermia in stroke patients with malignant infarction of the middle cerebral artery. Stroke 2001; 32:2833–2835. 66. Schwab S, Georgiadis D, Berrouschot J, et al. Feasibility and safety of moderate hypothermia after massive hemispheric infarction. Stroke 2001; 32:2033–2035. 67. Georgiadis D, Schwarz S, Aschoff A, et al. Hemicraniectomy and moderate hypothermia in patients with severe ischemic stroke. Stroke 2002; 33:1584– 1588. 68. Milhaud D, Thouvenot E, Heroum C, et al. Prolonged moderate hypothermia in massive hemispheric infarction: clinical experience. J Neurosurg Anesthesiol 2005; 17:49–53. 69. Els T, Oehm E, Voigt S, et al. Safety and therapeutical benefit of hemicraniectomy combined with mild hypothermia in comparison with hemicraniectomy alone in patients with malignant ischemic stroke. Cerebrovasc Dis 2006; 21:79–85. 70. Johnson RD, Maartens NF, Teddy PJ. Technical aspects of decompressive & craniectomy for malignant middle cerebral artery infarction. J Clin Neurosci 18:1023–1027. This is a detailed review of surgical practice of decompressive hemicraniectomy including complications. 71. Chung J, Bang OY, Lim YC, et al. Newly suggested surgical method of decompressive craniectomy for patients with middle cerebral artery infarction. Neurologist 2011; 17:11–15. 72. Fischer U, Taussky P, Gralla J, et al. Decompressive craniectomy after intraarterial thrombolysis: safety and outcome. J Neurol Neurosurg Psychiatry 2011; 82:885–887. 73. Staykov D, Gupta R. Hemicraniectomy in malignant middle cerebral artery infarction. Stroke 2011; 42:513–516. 74. Akins PT, Guppy KH. Sinking skin flaps, paradoxical herniation, and external brain tamponade: a review of decompressive craniectomy management. Neurocrit Care 2008; 9:269–276.

75. Sarov M, Guichard JP, Chibarro S, et al. Sinking skin flap syndrome and paradoxical herniation after hemicraniectomy for malignant hemispheric infarction. Stroke 2010; 41:560–562. This is a detailed description of symptoms, signs, treatment, and predictors of an important complication of hemicraniectomy. 76. Waziri A, Fusco D, Mayer SA, et al. Postoperative hydrocephalus in patients undergoing decompressive hemicraniectomy for ischemic or hemorrhagic stroke. Neurosurgery 2007; 61:489–493; discussion 493–484. 77. Rahme R, Weil AG, Sabbagh M, et al. Decompressive craniectomy is not an independent risk factor for communicating hydrocephalus in patients with increased intracranial pressure. Neurosurgery 2010; 67:675–678; discussion 678. 78. Cho DY, Chen TC, Lee HC. Ultra-early decompressive craniectomy for malignant middle cerebral artery infarction. Surg Neurol 2003; 60:227– 232; discussion 232–223. 79. Gupta R, Connolly ES, Mayer S, et al. Hemicraniectomy for massive middle cerebral artery territory infarction: a systematic review. Stroke 2004; 35:539– 543. 80. Mori K, Aoki A, Yamamoto T, et al. Aggressive decompressive surgery in patients with massive hemispheric embolic cerebral infarction associated with severe brain swelling. Acta Neurochir (Wien) 2001; 143:483–491; discussion 491–482. 81. Schwab S, Steiner T, Aschoff A, et al. Early hemicraniectomy in patients with complete middle cerebral artery infarction. Stroke 1998; 29:1888–1893. 82. Walz B, Zimmermann C, Bottger S, et al. Prognosis of patients after hemicraniectomy in malignant middle cerebral artery infarction. J Neurol 2002; 249:1183–1190. 83. Uhl E, Kreth FW, Elias B, et al. Outcome and prognostic factors of hemicraniectomy for space occupying cerebral infarction. J Neurol Neurosurg Psychiatry 2004; 75:270–274. 84. Frank JI CD, Thisted R, Kordeck C, et al. HeADDFIRST Trialists. Hemicraniectomy and durotomy upon deterioration from infarction related swelling trial (HeADDFIRST): First public presentation of the primary study findings. Abstract and Scientific Session, 55th Annual Meeting of the American Academy of Neurology, March 19–April 5, 2003. 85. Juttler E, Bosel J, Amiri H, et al. DESTINY II: DEcompressive Surgery for the Treatment of malignant INfarction of the middle cerebral arterY II. Int J Stroke 2011; 6:79–86. 86. Weil AG, Rahme R, Moumdjian R, et al. Quality of life following hemicraniectomy for malignant MCA territory infarction. Can J Neurol Sci 2011; 38:434–438. 87. Kelly AG, Holloway RG. Health state preferences and decision-making after malignant middle cerebral artery infarctions. Neurology 2010; 75:682–687. 88. Kiphuth IC, Kohrmann M, Lichy C, et al. Hemicraniectomy for malignant middle cerebral artery infarction: retrospective consent to decompressive surgery depends on functional long-term outcome. Neurocrit Care 2010; 13:380– 384. 89. Schmidt H, Heinemann T, Elster J, et al. Cognition after malignant & media infarction and decompressive hemicraniectomy – a retrospective observational study. BMC Neurol 2011; 11:77. This is one of the first comprehensive studies looking at neuropsychological outcome after hemicraniectomy. &

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