the influence of decompressive craniectomy for major ... · the influence of decompressive...

J Neurosurg Volume 123 • July 2015

cliNical articleJ Neurosurg 123:59–64, 2015

Although numerous aspects of decompressive cra-niectomy (DC) for major stroke are still under discussion, its beneficial effect on overall sur-

vival and clinical outcome is widely accepted nowadays. Multiple randomized clinical trials have shown improved survival and functional outcome in patients treated with DC compared with conservative or best medical treat-ment.10,11,15,21,24,31 Despite these findings patient selection and timing of surgery remain controversial.14,29

The pathophysiological background of DC in major stroke has been only sparsely investigated.2,6,23 An in-crease in cerebral perfusion pressure was shown follow-ing DC for traumatic brain injury.4 Perfusion improvement following DC for major stroke has been described, and whole-brain and penumbra perfusion improvement has been stated as a therapeutic target in DC in multiple publi-cations.5,14,24,31 An animal study investigating the effect of

DC in a rat model of stroke showed a significant reduction in final infarct size and an improvement in perfusion via leptomeningeal collateral vessels, as measured by MRI.5

Perfusion CT (PCT) is widely used in stroke imaging.18 It can be used to monitor penumbra perfusion, to detect additional infarction, and to monitor treatment success in revascularization.3,16,25

It can be postulated that DC is followed by an improve-ment in cerebral perfusion due to reduced general and lo-cal pressure. We therefore designed a study to investigate cerebral perfusion changes before and early after DC for major stroke by PCT.

MethodsPatient Population

The present study analyzed data from patients meet-

abbreviatioNs AU = arbitrary units; CBF = cerebral blood flow; CBV = cerebral blood volume; DC = decompressive craniectomy; ICP = intracranial pressure; MCA = middle cerebral artery; MTT = mean transit time; PCT = perfusion CT; Tmax = time to peak of the residue function.subMitted June 4, 2014. accePted December 2, 2014.iNclude wheN citiNg Published online January 30, 2015; DOI: 10.3171/2014.12.JNS141250.disclosure The authors report no conflict of interest concerning the materials or methods used in this study or the findings specified in this paper.

The influence of decompressive craniectomy for major stroke on early cerebral perfusionPhilipp Jörg slotty, Md,1,3 Marcel alexander Kamp, Md,1 thomas beez, Md,1 henrieke beenen,1 hans-Jakob steiger, Md,1 bernd turowski, Md,3 and daniel hänggi, Md1

Departments of 1Neurosurgery and 2Neuroradiology, Medical Faculty, Heinrich Heine University, Düsseldorf, Germany; and 3Division of Neurosurgery, Department of Surgery, University of British Columbia, Vancouver, British Columbia, Canada

obJect Multiple trials have shown improved survival and functional outcome in patients treated with decompressive craniectomy (DC) for brain swelling following major stroke. It has been assumed that decompression induces an im-provement in cerebral perfusion. This observational study directly measured cerebral perfusion before and after decom-pression.Methods Sixteen patients were prospectively examined with perfusion CT within 6 hours prior to surgery and 12 hours after surgery. Preoperative and postoperative perfusion measurements were compared and correlated.results Following DC there was a significant increase in cerebral blood flow in all measured territories and addition-ally an increase in cerebral blood volume in the penumbra (p = 0.03). These changes spread as far as the contralateral hemisphere. No significant changes in mean transit time or Tmax (time-to-peak residue function) were observed.coNclusioNs The presurgical perfusion abnormalities likely reflected local pressure-induced hypoperfusion with impaired autoregulation. The improvement in perfusion after decompression implied an increase in perfusion pressure, likely linked to partial restoration of autoregulation. The increase in perfusion that was observed might partially be re-sponsible for improved clinical outcome following decompressive surgery for major stroke. The predictive value of perfu-sion CT on outcome needs to be evaluated in larger trials.http://thejns.org/doi/abs/10.3171/2014.12.JNS141250KeY words stroke; decompressive craniectomy; cerebral perfusion; traumatic brain injury

59©AANS, 2015

Unauthenticated | Downloaded 10/04/20 01:39 PM UTC

P. J. slotty et al.

ing the following inclusion criteria: 1) acute supratentorial unilateral middle cerebral artery (MCA) territory infarc-tion, 2) selected for DC, 3) preoperative PCT scanning within 6 hours before surgery, 4) postoperative PCT scan-ning within 12 hours after DC, 5) patient age greater than 18 years, and 6) informed consent for study participation obtained from the patient or a legal representative.

The present study was reviewed and approved by the lo-cal institutional ethics review board of the medical faculty of the Heinrich Heine University, Düsseldorf, Germany.

Exclusion criteria were 1) hemorrhagic infarction, 2) multi-territorial stroke, 3) admission more than 12 hours after onset, 4) pregnancy, 5) clotting disorders, and 6) sur-gical complications.

study designFor patients allocated to the present analysis, a stan-

dardized PCT screening protocol was performed immedi-ately after admission. The management of these patients, their selection for DC, and the surgical procedure itself were in accordance with current international guide-lines.13,28,30 After the decompressive surgery, the patients enrolled in this study underwent a second PCT study in addition to the routine postoperative CT scan. Preopera-tive and postoperative perfusion measurements were com-pared and correlated.

PCT Methods and DefinitionsAs previously described, 360° cortical banding analy-

sis and singular value decomposition were used for cal-culation of PCT data such as mean transit time (MTT), time to peak of the residue function (Tmax), cerebral blood flow (CBF), and cerebral blood volume (CBV).26,27 The PCT acquisition time was 50 seconds. After genera-tion of perfusion maps using the software stroketool-CT (Version 2.0, www.digitalimagesolutions.de), the ischemic tissue was determined by the steep decrease in CBF as described in previous publications.7,8 The penumbra was defined as the area adjacent to the ischemic tissue, where the CBF showed an increase before reaching the plateau of perfusion in the non-ischemic brain; this area extended for approximately 10°–15° in both the anterior and posterior directions (Fig. 1). The rest of the hemisphere ipsilateral to the stroke, excluding the ischemic core, was defined as ipsilateral residual hemisphere. The contralateral hemi-sphere was also analyzed. Volumetric calculations were conducted using 3DSlicer (freeware, www.slicer.org) seg-mentation and quantification routines.

statistical analysisStatistical analyses were performed using SPPS Version

19 (IBM Corp.) and GraphPad prism (GraphPad Software Inc.). Paired t-tests were performed for pre- and post-DC comparisons following verification of normal distribution by Kolmogorov-Smirnov test. Results given are arithmetic means for continuous variables unless otherwise stated. The level of significance was stipulated as 0.05.

MTT and Tmax are given in deciseconds (dsec); CBV and CBF are relative parameters and are therefore given in arbitrary units (AU).

resultsgeneral

Twenty-nine patients underwent DC for the treatment of major stroke at a German university tertiary care center from November 2011 to January 2013.

Ten patients were excluded because of missing or out-of-time-frame imaging and 3 patients were excluded due to hemorrhages. Overall, 32 PCT maps obtained in 16 pa-tients treated by DC for major stroke between 2011 and 2013 were included in this analysis. The study group in-cluded 6 women and 10 men, and the patients’ mean age was 50.2 years (SD 9.2 years). Eight patients suffered a right MCA stroke and 8 a left MCA stroke; 1 patient had a partial MCA infarction plus a posterior cerebral artery infarction.

The mean volume of infarction determined by clearly demarcated tissue in pre-DC CT imaging was 213.2 cm3 (SD 77.4 cm3). The mean time between onset of symp-toms and surgery was 33.7 hours, and the median Glasgow Coma Scale score at initiation of surgery was 9 (range 3–15). The median time between DC and postsurgery PCT was 8.3 hours (SD 2.4 hours).

Perfusion changes in the PenumbraReflecting close-range effects of DC, the penumbra

was defined as the area of perfusion changes between is-chemic tissue and brain not affected or only remotely af-

Fig. 1. Example of an MTT map showing the regions of interest mea-sured. The green subcortical band represents the area actually mea-sured. The area indicated by A (red) is the ischemic zone; B (yellow), the penumbra; C + B (blue + yellow), the ipsilateral residual hemisphere; and D (orange), the contralateral hemisphere. The venous sinuses are excluded. Figure is available in color online only.



Perfusion after dc for major stroke

fected by the ischemic event, as indicated by stable CBF values. This technique resulted in the identification of re-gions adjacent to the ischemic tissue extending 10°–15° in the anterior and posterior directions (Fig. 1). A mean decrease in MTT of 2.41 dsec in the penumbra was ob-served, although this difference did not reach statistical significance (p = 0.454). Similar findings were evident for Tmax, with a mean decrease of 7.86 dsec (p = 0.274).

CBF and CBV both showed a significant increase fol-lowing DC (15.02 AU for CBF, p = 0.014; 3.86 AU for CBV, p = 0.030; Table 1, Fig. 2).

Perfusion changes in the ipsilateral residual hemisphereTo determine medium-range effects of DC, the ipsilat-

eral residual hemisphere—excluding the ischemic area but including the penumbra—was also analyzed.

Similar effects as for the penumbra were observed. De-creases in MTT (5.95 dsec, p = 0.067) and Tmax (8.19 dsec, p = 0.068) were observed, although neither of these changes were statistically significant. CBF was signifi-cantly increased (9.62 AU, p = 0.037); CBV was slightly increased, although the increase did not reach statistical significance (0.81 AU, p = 0.653) following DC (Table 2, Fig. 2).

Perfusion changes in the contralateral hemisphereRemote effects of space-occupying infarction on ce-

rebral perfusion are a likely explanation of clinical dete-rioration not explained by local ischemia. In the contralat-eral hemisphere a marked increase in CBF was observed (20.96 AU, p = 0.006). A decrease in MTT and Tmax and a slight increase in CBV were observed, although the differ-ence did not reach statistical significance (Table 3, Fig. 2).

clinical outcomeThe median follow-up was 20.8 months (SD 7.6

months), and the median modifed Rankin Scale score at most recent follow-up was 4 with a Barthel Index score of 27 (SD 26). Two patients died during the follow-up pe-riod, and in both cases death was due to coronary events. Eleven patients underwent cranioplasty following reha-bilitation; 9 patients received an autologous implant and 2 an artificial implant. Three patients required permanent CSF shunting.

discussionOur findings showed that distinct and consistent short-

term effects of DC on cerebral perfusion can be measured by PCT: 1) an increase in CBF was observed in all regions investigated, 2) an increase in CBV was observed in the vicinity of the infarction, and 3) MTT and Tmax were not significantly influenced by DC.

The changes in CBF and CBV were concentrated in, but not limited to, the penumbra and the ipsilateral re-sidual hemisphere and spread as far as the contralateral hemisphere.

Our present observations are only partially in line with the findings of a recently published study of 29 patients treated by DC for malignant stroke, in which Amorim et al. found that DC significantly improved MTT in the con-tralateral hemisphere and penumbra and CBF in the whole

brain, but not MTT or CBV in the ipsilateral hemisphere.1 In contrast, MTT and Tmax were not significantly influ-enced in our series, but CBF was changed in all regions in-vestigated, and CBV was changed in the vicinity of the in-farction. A decrease in MTT and also Tmax was observed in the ipsilateral residual hemisphere and a decrease in MTT was observed in the contralateral hemisphere, al-though these decreases did not reach significance. A larger patient population would likely lead to significant results. Reduced cerebrovascular reserve capacity and reduced overall CBF and CBV in older patients are a likely ex-planation for the observed worse clinical outcome in the elderly.12,18,19,21,33 Interestingly, hemodynamic benefit was barely evident after DC for patients older than 55 years in the publication by Amorim et al.,1 and the differences observed in the hemodynamic PCT parameters might be explained by an older patient population in our series. Timing of surgery is another factor known to significantly influence the outcome of DC for stroke and will most like-ly impact PCT results.17

Our results are in line with the first description of PCT measurement before and after DC for stroke published by Bendzsus et al. in 2003.2 In their case report they ob-served an increase in CBF and CBV in the penumbra and a decrease in Tmax following DC, but they did not offer a pathophysiological explanation for their observations.

Relative MTT as a tissue-specific marker was consid-ered as a surrogate for final infarct size after ischemic stroke and for prediction of perfusion impairment dur-ing delayed cerebral ischemia after subarachnoid hem-orrhage.27,32 MTT—in combination with other perfusion parameters—is believed to be an accurate marker for pre-diction of cerebral ischemia.9 However, cerebral perfusion changes after DC for malignant stroke should be patho-physiologically comparable to perfusion changes during cerebral hematoma evacuation. In the study by Etminan et al., MTT was globally elevated in both hemispheres ini-tially and did not improve in either hemisphere after surgi-cal hematoma removal.8 In contrast, Tmax, CBF, and CBV were impaired in the perihematomal zone and resolved after hematoma evacuation.

Similar results were observed in the current series but likely for different reasons: as in the perihematomal zone of intracerebral hemorrhage, pre-DC perfusion in the pen-umbra and the ipsilateral residual hemisphere might not only be affected by cerebral hypoperfusion due to low ce-rebral perfusion pressure but also by pressure effects hin-dering autoregulation.

Clinically these assumptions are supported by the com-monly observed rapid improvement in neurological state following DC and reports on neurological improvement by anti-edema therapy with mannitol.2

table 1. Perfusion parameter statistics before and after dc: penumbra

Parameter Mean Difference 95% CI p Value

MTT (dsec) −2.41 −4.28 to 9.11 0.454Tmax (dsec) −7.86 −6.90 to 22.63 0.274CBF (AU) 15.02 −26.54 to −3.49 0.014CBV (AU) 3.86 −7.29 to −0.43 0.030

J Neurosurg Volume 123 • July 2015 61


P. J. slotty et al.

Reduction of CBF and CBV prior to DC is thought to be a surrogate for local pressure on the microvasculature, reduced cerebral perfusion pressure, and impaired auto-regulation. Increase in both parameters after DC might represent an increase in cerebral perfusion pressure, likely accompanied by the restoration of autoregulation. The dis-tinct rise in CBV in the penumbra might resemble early vasoparalysis following surgery or reactive hyperperfu-sion in the penumbra. This post-ischemic hyperperfusion has long been thought to be of detrimental effect, although this assumption is still under discussion.20 Therefore the effect of CBF and CBV increase on functional outcome cannot be conclusively assessed.

Venous outflow obstruction due to increased local or global intracranial pressure resulting in venous congestion can be discussed as an additional pathomechanism. Ve-nous pooling or stasis effects cannot be measured directly by PCT, therefore no evaluation of this mechanism can be given. But low pre-DC CBV values and the post-DC increase in CBF and CBV suggest reduced arterial inflow with reduced overall blood volume in the penumbra prior to decompression.

Reduced mortality and reduced morbidity might be triggered by two different effects of DC in major stroke. Mortality reduction is most likely induced by prevention of herniation, while morbidity reduction might at least be in some part induced by improvement of penumbra and overall brain perfusion resulting in a reduction of addi-tional tissue damage beyond the immediate ischemic zone. This assumption might help to interpret results from past and future clinical trials in DC for major stroke, es-pecially regarding the observed significant differences in populations of different ages.

Neurological deficits exceeding functions located in the ischemic area are commonly observed in patients suf-fering from major stroke. Models of explanation include but are not limited to accumulation of toxic metabolites, hydrocephalus, and global hypoperfusion.22 We observed remote perfusion changes in the contralateral hemisphere including a high MTT prior to DC and a significant in-crease in CBF following DC. These remote changes are most likely a response to intracranial pressure (ICP) de-crease followed by an increase in cerebral perfusion pres-sure. This effect has been shown to occur in decompres-

table 2. Perfusion parameter statistics before and after dc: ipsilateral residual hemisphere


MTT (dsec) −5.95 −0.47 to 12.38 0.067Tmax (dsec) −8.19 −0.68 to 17.06 0.068CBF (AU) 9.62 −18.60 to −0.65 0.037CBV (AU) 0.81 −4.61 to 2.97 0.653

table 3. Perfusion parameter statistics before and after dc: contralateral hemisphere


MTT (dsec) −3.92 −0.82 to 8.67 0.098Tmax (dsec) −0.67 −3.87 to 5.22 0.756CBF (AU) 20.96 −34.87 to −7.05 0.006CBV (AU) 3.03 −6.30 to 0.23 0.067

Fig. 2. Time course of measured perfusion parameters before and after DC in the contralateral hemisphere (a), penumbra (b), and ipsilateral re-sidual hemisphere (c). Time is given in deciseconds on the y-axis for MTT and Tmax; CBV and CBF are relative values given in arbitrary units.



Perfusion after dc for major stroke

sion for traumatic brain injury.4 Additionally, this finding provides a possible explanation for neurological deficits in-volving functions other than those located in the ischemic area and loss of consciousness in patients without signs of herniation. Protection of the hemisphere contralateral to the stroke is a strong argument for early decompression.

The parameter thought to best reflect increased ICP is Tmax. Tmax is known to be mainly influenced by blood inflow—e.g., decreased carotid artery inflow due to de-creased cerebral perfusion pressure. The slight decrease in Tmax observed throughout the areas investigated likely results from decompression-induced general ICP reduc-tion. This can only be assumed, as no data on pre-DC ICP are available.

Besides missing data on ICP we acknowledge some fur-ther limitations to our study. 1) The study included a rela-tively small number of patients. 2) PCT only provides rela-tive values on the most interesting parameters, CBF and CBV. Absolute CBF and CBV values, which it is possible to measure (e.g., by using xenon-enhanced perfusion im-aging), would reveal additional information and might pro-vide decision guidance for surgery. 3) No additional PCT measurements were performed during the later course of the disease, and such measurements might have allowed deeper insight into the intermediate and long-term effects of DC in this patient group. 4) No perfusion data from pa-tients not undergoing DC were available for comparison.

A correlation of clinical outcome and perfusion param-eter changes was not performed in our study, as a meaning-ful analysis would require much higher patient numbers. Based on the findings presented in this study we expect a clinical relation to exist and adding PCT to further studies on DC in cerebral infarction might provide deeper insight into this intriguing subject.

conclusionsDistinct perfusion changes can be observed in PCT im-

aging immediately before and after decompressive crani-ectomy (DC) for major stroke.

Perfusion improvement is not limited to the penumbra. Similar effects can be observed in the residual ipsilateral and contralateral hemispheres. The pre-DC changes ob-served most likely reflect pressure-induced hypoperfu-sion. Post-DC perfusion improvement implies increased cerebral perfusion pressure, likely accompanied by incipi-ent restoration of autoregulation. The increase in perfu-sion observed might be partially responsible for improved clinical outcome. The predictive value of PCT still has to be evaluated in larger trials.

references 1. Amorim RL, de Andrade AF, Gattás GS, Paiva WS, Menezes

M, Teixeira MJ, et al: Improved hemodynamic parameters in middle cerebral artery infarction after decompressive crani-ectomy. Stroke 45:1375–1380, 2014

2. Bendszus M, Müllges W, Goldbrunner R, Weigand A, Soly-mosi L: Hemodynamic effects of decompressive craniotomy in MCA infarction: evaluation with perfusion CT. Eur Ra-diol 13:1895–1898, 2003

3. Beseoglu K, Etminan N, Turowski B, Steiger HJ, Hänggi D: The extent of the perihemorrhagic perfusion zone correlates

with hematoma volume in patients with lobar intracerebral hemorrhage. Neuroradiology 56:535–541, 2014

4. Bor-Seng-Shu E, Figueiredo EG, Amorim RL, Teixeira MJ, Valbuza JS, de Oliveira MM, et al: Decompressive craniec-tomy: a meta-analysis of influences on intracranial pressure and cerebral perfusion pressure in the treatment of traumatic brain injury. J Neurosurg 117:589–596, 2012

5. Doerfler A, Engelhorn T, Heiland S, Benner T, Forsting M: Perfusion- and diffusion-weighted magnetic resonance imag-ing for monitoring decompressive craniectomy in animals with experimental hemispheric stroke. J Neurosurg 96:933–940, 2002

6. Engelhorn T, Doerfler A, de Crespigny A, Beaulieu C, Forsting M, Moseley ME: Multilocal magnetic resonance perfusion mapping comparing the cerebral hemodynamic effects of decompressive craniectomy versus reperfusion in experimental acute hemispheric stroke in rats. Neurosci Lett 344:127–131, 2003

7. Etminan N, Beseoglu K, Heiroth HJ, Turowski B, Steiger HJ, Hänggi D: Early perfusion computerized tomography imag-ing as a radiographic surrogate for delayed cerebral ischemia and functional outcome after subarachnoid hemorrhage. Stroke 44:1260–1266, 2013

8. Etminan N, Beseoglu K, Turowski B, Steiger HJ, Hänggi D: Perfusion CT in patients with spontaneous lobar intracere-bral hemorrhage: effect of surgery on perihemorrhagic per-fusion. Stroke 43:759–763, 2012

9. Ford AL, An H, Kong L, Zhu H, Vo KD, Powers WJ, et al: Clinically relevant reperfusion in acute ischemic stroke: MTT performs better than Tmax and TTP. Transl Stroke Res 5:415–421, 2014

10. Geurts M, van der Worp HB, Kappelle LJ, Amelink GJ, Algra A, Hofmeijer J: Surgical decompression for space-occupying cerebral infarction: outcomes at 3 years in the randomized HAMLET trial. Stroke 44:2506–2508, 2013

11. Hofmeijer J, Kappelle LJ, Algra A, Amelink GJ, van Gijn J, van der Worp HB: Surgical decompression for space-occupy-ing cerebral infarction (the Hemicraniectomy After Middle Cerebral Artery infarction with Life-threatening Edema Trial [HAMLET]): a multicentre, open, randomised trial. Lancet Neurol 8:326–333, 2009

12. Holtkamp M, Buchheim K, Unterberg A, Hoffmann O, Schielke E, Weber JR, et al: Hemicraniectomy in elderly patients with space occupying media infarction: improved survival but poor functional outcome. J Neurol Neurosurg Psychiatry 70:226–228, 2001

13. Jauch EC, Saver JL, Adams HP Jr, Bruno A, Connors JJ, De-maerschalk BM, et al: Guidelines for the early management of patients with acute ischemic stroke: a guideline for health-care professionals from the American Heart Association/American Stroke Association. Stroke 44:870–947, 2013

14. Jüttler E, Hacke W: Early decompressive hemicraniectomy in older patients with nondominant hemispheric infarction improves outcome. Stroke 42:843–844, 2011

15. Jüttler E, Schwab S, Schmiedek P, Unterberg A, Hennerici M, Woitzik J, et al: Decompressive Surgery for the Treat-ment of Malignant Infarction of the Middle Cerebral Ar-tery (DESTINY): a randomized, controlled trial. Stroke 38:2518–2525, 2007

16. Kan P, Snyder KV, Binning MJ, Siddiqui AH, Hopkins LN, Levy EI: Computed tomography (CT) perfusion in the treat-ment of acute stroke. World Neurosurg 74:550–551, 2010

17. Kilincer C, Asil T, Utku U, Hamamcioglu MK, Turgut N, Hicdonmez T, et al: Factors affecting the outcome of decom-pressive craniectomy for large hemispheric infarctions: a prospective cohort study. Acta Neurochir (Wien) 147:587–594, 2005

18. Koenig M, Kraus M, Theek C, Klotz E, Gehlen W, Heuser L: Quantitative assessment of the ischemic brain by means

J Neurosurg Volume 123 • July 2015 63


P. J. slotty et al.

of perfusion-related parameters derived from perfusion CT. Stroke 32:431–437, 2001

19. Lartaud I, Bray-des-Boscs L, Chillon JM, Atkinson J, Capdeville-Atkinson C: In vivo cerebrovascular reactivity in Wistar and Fischer 344 rat strains during aging. Am J Physiol 264:H851–H858, 1993

20. Marchal G, Young AR, Baron JC: Early postischemic hyper-perfusion: pathophysiologic insights from positron emission tomography. J Cereb Blood Flow Metab 19:467–482, 1999

21. Molina CA, Selim MH: Decompressive hemicraniectomy in elderly patients with malignant hemispheric infarction: open questions remain beyond DESTINY. Stroke 42:847–848, 2011

22. Saunders DE, Howe FA, van den Boogaart A, McLean MA, Griffiths JR, Brown MM: Continuing ischemic damage after acute middle cerebral artery infarction in humans demon-strated by short-echo proton spectroscopy. Stroke 26:1007–1013, 1995

23. Schaller B, Graf R, Sanada Y, Rosner G, Wienhard K, Heiss WD: Hemodynamic and metabolic effects of decompressive hemicraniectomy in normal brain. An experimental PET-study in cats. Brain Res 982:31–37, 2003

24. Schwab S, Steiner T, Aschoff A, Schwarz S, Steiner HH, Jan-sen O, et al: Early hemicraniectomy in patients with complete middle cerebral artery infarction. Stroke 29:1888–1893, 1998

25. Turk A, Magarik JA, Chaudry I, Turner RD, Nicholas J, Hol-mstedt CA, et al: CT perfusion-guided patient selection for endovascular treatment of acute ischemic stroke is safe and effective. J Neurointerv Surg 4:261–265, 2012

26. Turowski B, Haenggi D, Wittsack HJ, Beck A, Aurich V: [Computerized analysis of brain perfusion parameter im-ages.] Rofo 179:525–529, 2007 (Ger)

27. Turowski B, Haenggi D, Wittsack J, Beck A, Moedder U: [Cerebral perfusion computerized tomography in vasospasm after subarachnoid hemorrhage: diagnostic value of MTT.] Rofo 179:847–854, 2007 (Ger)

28. Vahedi K, Hofmeijer J, Juettler E, Vicaut E, George B, Algra A, et al: Early decompressive surgery in malignant infarction of the middle cerebral artery: a pooled analysis of three ran-domised controlled trials. Lancet Neurol 6:215–222, 2007

29. van der Worp HB, Kappelle LJ: Early decompressive hemi-craniectomy in older patients with nondominant hemispheric infarction does not improve outcome. Stroke 42:845–846, 2011

30. Vertinsky P: Physique as destiny: William H. Sheldon, Bar-bara Honeyman Heath and the struggle for hegemony in the science of somatotyping. Can Bull Med Hist 24:291–316, 2007

31. Vibbert M, Mayer SA: Early decompressive hemicraniec-tomy following malignant ischemic stroke: the crucial role of timing. Curr Neurol Neurosci Rep 10:1–3, 2010

32. Wintermark M, Flanders AE, Velthuis B, Meuli R, van Leeuwen M, Goldsher D, et al: Perfusion-CT assessment of infarct core and penumbra: receiver operating characteristic curve analysis in 130 patients suspected of acute hemispheric stroke. Stroke 37:979–985, 2006

33. Wollner L, McCarthy ST, Soper ND, Macy DJ: Failure of cerebral autoregulation as a cause of brain dysfunction in the elderly. BMJ 1:1117–1118, 1979

authors contributionsConception and design: Slotty, Hänggi. Acquisition of data: Slotty, Beez, Beenen, Turowski. Analysis and interpretation of data: Slotty, Kamp, Beez, Beenen, Turowski, Hänggi. Drafting the article: Slotty. Critically revising the article: Slotty, Kamp, Beez, Steiger, Hänggi. Reviewed submitted version of manu-script: all authors. Approved the final version of the manuscript on behalf of all authors: Slotty. Statistical analysis: Slotty. Administrative/technical/material support: Beenen, Steiger, Turowski. Study supervision: Slotty, Hänggi.

correspondencePhilipp J. Slotty, Gordon & Leslie Diamond Health Care Centre, Vancouver General Hospital, 8101-2775 Laurel St., Vancouver, BC V5Z 1M9, Canada. email: [email protected].



the influence of decompressive craniectomy for major ... · the influence of decompressive...

Documents