(Stroke. 2001;32:813.)
© 2001 American Heart Association, Inc.
Letters to the Editor |
Decompressive Craniectomy for Early Therapy and Secondary Prevention of Cerebral Infarction
Department of Neuroradiology, University of Essen Medical School, Essen, Germany
To the Editor:
We read with great interest the recent article by Oppenheim and colleagues.1 The authors reported a small, retrospective series of 28 patients at high risk of developing malignant middle cerebral artery (MCA) infarction and identified quantitative volume measurement of diffusion-weighted imaging (DWI) ischemic hyperintensity as a reliable tool to predict malignant MCA infarction.
Ischemic cerebral infarction associated with extensive edema and marked elevation of intracranial pressure may cause ischemia of neighboring brain tissue and thus lead to further infarction.2 Decompressive craniectomy may interrupt this vicious cycle by decreasing intracranial pressure. This may increase cerebral perfusion pressure and optimize retrograde perfusion of MCA branches via leptomeningeal collaterals; functionally compromised but viable brain may thus be able to survive.3
The clinical4 and our experimental5 6 7 results indicate that decompressive craniectomy for space-occupying cerebral ischemia not only reduces mortality but also significantly improves outcome and reduces infarction size, especially when performed very early after vessel occlusion. MR studies revealed a better retrograde perfusion via leptomeningeal collaterals as possible mechanisms for reduced infarction volume in our early-treated animals.7 8
In addition to the authors, we would like to draw particular attention to the primary goal of decompressive craniectomy: not only to be livesaving, but also to achieve survival in an acceptable clinical condition. Our experimental results indicate that decompressive craniectomy as an early secondary prevention of cerebral infarction may limit the further evolution of cerebral ischemia. Clinically, hemicraniectomy is technically a simple procedure that can be performed with minimal ancillary support, and in contrast to thrombolytic therapy, without increased risk of intracerebral hemorrhage.9
However, one problem facing the clinician is to determine the length of time to continue conservative therapy before considering an invasive therapy such as craniectomy. For early and probably most effective treatment, the "malignant" character of the ischemic lesion has to be recognized during the first hours after the onset of symptoms. We agree with the authors that an early predictor of malignant hemispheric infarction would be desirable and of crucial value for the further therapeutic management of these patients. Clinical signs such as hemiparesis and coma are neither signs nor indicators of a "malignant" hemispheric stroke. Intracranial pressure monitoring is invasive and partially unreliable. Conventional imaging methods such as CT or T1- and T2-weighted MRI are insensitive in this early stage.10 11 The unique advantage of MRI is the possibility of obtaining multimodal information of the ischemic tissue with a single imaging modality. The combination of perfusion-weighted imaging (PWI) and DWI ("mismatch") provides information on the "tissue at risk" as a time-independent marker, individually for each patient.12 We therefore wonder why the authors did not perform MR perfusion measurements. Considering patient selection for craniectomy, it is of crucial value to know this extent of the tissue at risk. Using DWI alone, appropriate patient selection is difficult, concerning the primary goal of early ischemic therapy. Additionally, an absolute cutoff value of DWI ischemic hyperintensity may be not sufficient to characterize the complex and dynamic process of cerebral ischemia.
We believe that in the future, imaging techniques such as perfusion and diffusion MRI may enable determination of the clinical significance of cerebral ischemia early after onset, thereby allowing initiation of aggressive treatment forms, such as craniectomy, before life-threatening brain swelling and herniation occur. The retrospective study by Oppenheim and colleagues is one important step in this direction. However, further prospective studies are necessary to determine valid predictors and threshold values for malignant cerebral infarction.
References
1.
Oppenheim
C, Samson Y, Manai R, Lalam T, Vandamme X, Crozier S, Srour A, Cornu P,
Dormont D, Rancurel G, Marsault C. Prediction of malignant middle
cerebral artery infarction by diffusion-weighted imaging.
Stroke. 2000;31:2175–2181.
2.
Hacke W, Schwab S,
Horn M, Spranger M, De Georgia M, von Kummer R. The "malignant"
middle cerebral artery territory infarction: clinical course and
prognostic signs. Arch Neurol. 1996;53:309–315.
3. Forsting M, Krieger D, von Kummer R, Hacke W, Sartor K. The prognostic value of collateral blood flow in acute middle cerebral artery occlusion. In: del Zoppo GJ, Mori E, Hacke W, eds. Thrombolytic Therapy in Acute Ischemic Stroke II. Heidelberg, Germany: Springer-Verlag; 1993:160–167.
4.
Schwab S, Steiner
T, Aschoff A, Schwarz S, Steiner HH, Jansen O, Hacke W. Early
hemicraniectomy in patients with complete middle cerebral artery
infarction. Stroke. 1998;29:1888–1893.
5.
Forsting M, Reith
W, Schaebitz WR, Heiland S, von Kummer R, Hacke W, Sartor K.
Decompressive craniectomy for cerebral infarction: an experimental
study in rats. Stroke. 1995;26:259–264.
6. Doerfler A, Forsting M, Reith W, Staff C, Heiland S, Schaebitz WR, von Kummer R, Hacke W, Sartor K. Decompressive craniectomy in a rat model of "malignant" cerebral hemispheric stroke: experimental support for an aggressive approach. J Neurosurg. 1996;85:853–859.[Medline] [Order article via Infotrieve]
7.
Engelhorn T,
Doerfler A, Beaulieu C, Kastrup A, De Crespigny A, Forsting M, Moseley
ME. Reperfusion decompressive craniectomy or a combination of both: an
MRI-based study in rats.
Stroke. 1999;30:1456–1463.
8. Doerfler A, Engelhorn T, Heiland S, von Kummer R, Forsting M. Perfusion-MRI for monitoring of decompressive craniectomy in experimental hemispheric stroke. Stroke. 1999;30:275. Abstract P41.
9. Hacke W, Brott T, Caplan L, Meier D, Fieschi C, von Kummer R, Donnan G, Heiss WD, Wahlgren NG, Spranger M, Boysen G, Marler JR. Thrombolysis in acute ischemic stroke: controlled trials and clinical experience. Neurology. 1999;53:S3–S14.
10. Crain MR, Yuh WTC, Greene GM, Loes DJ, Ryals TJ, Sato Y, Hart MN. Cerebral ischemia: evaluation with contrast-enhanced MR imaging. AJNR Am J Neuroradiol. 1991;12:631–639.[Abstract]
11. Yuh WTC, Crain MR, Loes DJ, Grenne GM, Ryals TJ, Sato Y. MR imaging of cerebral ischemia: findings in the first 24 hours. AJNR Am J Neuroradiol. 1991;12:621–629.[Abstract]
12.
Schlaug G,
Benfield B, Baird A, Siewert B, Lovblad K, Parker R, Edelman R, Warach
S. The ischemic penumbra: operationally defined by diffusion
and perfusion MRI. Neurology.. 1999;53:1528–1537.
Response
Department of Neuroradiology
Department of Stroke Neurology, The Salpêtrière Hospital, Paris, France
We thank Doerfler et al for their letter concerning our article about DWI prediction of malignant MCA infarction.R1 We agree that the 145-cm3 threshold volume needs to be confirmed by a prospective study. We are now planning such a prospective study, and we will be happy to hear about any center interested in collaborating in such a study (contact: yves.samson@psl.ap-hop-paris.fr). As stated by Doerfler et al, we believe that hemicraniectomy may now be considered an established "lifesaving" procedure, but we think that further studies are still necessary to fully assess functional outcome of hemicraniectomy. Finally, Doerfler et al suggested that combining perfusion imaging with DWI would be of greater value than DWI alone in predicting the risk of malignant edema. It may well be, and we would be delighted to hear about data supporting this hypothesis. In our experience, however, it is not always possible to obtain reliable perfusion measurements in restless, acutely ill patients such as those included in our "malignant" group; even with the currently available postprocessing tools, perfusion MR still has some limitations. In addition, the DWI-perfusion mismatch is only an approximation of the ischemic penumbra and is more likely to reflect the "true penumbra" when DWI hyperintensity is small rather than large. We have concerns about the pathophysiological and clinical significance of the mismatch when the average volume of DWI hyperintensity already reaches 244 cm3, as was the case in our malignant group.
References
1. Oppenheim C, Samson Y, Manai R, Lalam T, Vandamme X, Crozier S, Srour A, Cornu P, Dormont D, Rancurel G, Marsault C. Prediction of malignant middle cerebral artery infarction by diffusion-weighted imaging. Stroke. 2000;31:2175–2181.
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