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Cerebral Edema associated with intracranial tumors
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8.
9. 10.
11.
Surg Neurol 1987;27:64-8
meningioma: CT and histological criteria including a new CT sign. AJNR 1982;3:267-76. Philippon J, Foncin JF, Grob R, Srour A, Poisson M, Pertuiset BF. Cerebral edema associated with meningiomas: possible role of a secretory-excretory phenomenon. Neurosurgery 1984;14:295-301. Russel DS, Rubinstein LJ. Pathology of tumors of the nervous system. 4th ed. Baltimore: Williams & Wilkins, 1977. Sigel RM, Messina AV. Computed tomography: the anatomical basis of the zone of diminished density surrounded meningiomas. AJR 1976;127:139-41. Smith HP, Challa VR, Moody DM, Kelly DL. Biological features
Maiuri et al
in meningiomas that determine the production of cerebral edema. Neurosurgery 1981;8:428-33. 12. Stevens JM, Ruiz JS, Kendall BE. Observation on peritumoral oedema in meningiomas. Part I: distribution, spread and extension of vasogenic edema seen on computed tomography. Neuroradiology 1983;25:71-80. 13. Stevens JM, Ruiz JS, Kendall BE. Observation on peritumoral oedema in meningioma. Part II: mechanisms of oedema production. Neuroradiology 1983;25:125-31. 14. Vassilouthis J, Ambrose J. Computerized tomography scanning appearances in intracranial meningiomas: an attempt to predict the histological features. J Neurosurg 1979;50:320-7.
Requested Editorial Cerebral Edema Associated with Intracranial Tumors
This article by Maiuri and colleagues on the relationship between the biologic features of meningiomas and their sometimes-critical associated cerebral edema draws our attention to a clinically important subject which deserves serious investigation. Klatzo [ 1] classified cerebral edema into cytotoxic and vasogenic types. The cerebral edema associated with intracranial tumors is vasogenic in origin. Other than anecdotal references to the severity of edema associated with fast-growing metastatic tumors and gliomas, most textbooks on neuropathology and neurosurgery contain little information about the mechanisms o f its production. Granted, the ultimate event is the breakdown of the blood-brain barrier (BBB) with leakage of plasma, but what are the other factors involved? It appears that the growth rate of the tumor may be important. It is known that malignant gliomas alter the BBB more than slow-growing benign gliomas and hence, are associated with more edema. However, studies of the cell-cycle kinetics of meningiomas or other tumors are needed to relate their growth characteristics with the amount of associated cerebral edema. The size of the tumor may be important in some cases. C a n large tumors cause cerebral edema solely by their size, even if their growth rate is slow? An analogy can be drawn here with subdural hematomas. Chronic subdural hematomas, presumably caused by repeated small episodes of rebleeding, can grow larger than acute subdural hematomas and yet can be associated with less edema than the latter. Again, a need to put together growth characteristics and size is evident. Do tumors secrete edemogenic substances? N o firm evidence is available to support this hypothesis, other than one paper cited by Maiuri et al that suggests such a mechanism.
Do tumor metabolites such as necrotic cells, polyamines, and D N A cause cerebral edema? Such possibilities exist with intraaxial tumors, but are unlikely to operate in noninvasive meningiomas. It has been suggested that some meningiomas, and perhaps other tumors, cause cerebral edema by compression of superficial veins and/or venous sinuses. One can only surmise that this happens in a few cases. Angiographic studies of tumors that are likely to compress veins may shed more light on this issue. Those interested in central nervous system neoplasia should be aware that cerebral edema associated with intracranial tumors may be multifactorial. The cause of edema in one patient may be different from that of another. Much work needs to be done, especially because improvements in the drug treatment of cerebral edema may depend on such studies. In the lung and the brain, edema can kill or seriously damage the patient. There is evidence that myelin sheaths may break down due to chronic edema. Herniation phenomena are clinically dangerous. Preoperative morbidity, operative difficulties and slow or incomplete postoperative recovery can all be traced to this complication. Cerebral edema associated with meningiomas in particular, and intracranial tumors in general, needs more scientific investigation. VENKATA R. CHALLA, M.D. Winston-Salem, North Carolina
Reference I. Klatzo 1. Neuropathological aspects of brain edema. J Neuropathol Exp Neurol 1967;26:1-14.
8.
9. 10.
11.
Surg Neurol 1987;27:64-8
meningioma: CT and histological criteria including a new CT sign. AJNR 1982;3:267-76. Philippon J, Foncin JF, Grob R, Srour A, Poisson M, Pertuiset BF. Cerebral edema associated with meningiomas: possible role of a secretory-excretory phenomenon. Neurosurgery 1984;14:295-301. Russel DS, Rubinstein LJ. Pathology of tumors of the nervous system. 4th ed. Baltimore: Williams & Wilkins, 1977. Sigel RM, Messina AV. Computed tomography: the anatomical basis of the zone of diminished density surrounded meningiomas. AJR 1976;127:139-41. Smith HP, Challa VR, Moody DM, Kelly DL. Biological features
Maiuri et al
in meningiomas that determine the production of cerebral edema. Neurosurgery 1981;8:428-33. 12. Stevens JM, Ruiz JS, Kendall BE. Observation on peritumoral oedema in meningiomas. Part I: distribution, spread and extension of vasogenic edema seen on computed tomography. Neuroradiology 1983;25:71-80. 13. Stevens JM, Ruiz JS, Kendall BE. Observation on peritumoral oedema in meningioma. Part II: mechanisms of oedema production. Neuroradiology 1983;25:125-31. 14. Vassilouthis J, Ambrose J. Computerized tomography scanning appearances in intracranial meningiomas: an attempt to predict the histological features. J Neurosurg 1979;50:320-7.
Requested Editorial Cerebral Edema Associated with Intracranial Tumors
This article by Maiuri and colleagues on the relationship between the biologic features of meningiomas and their sometimes-critical associated cerebral edema draws our attention to a clinically important subject which deserves serious investigation. Klatzo [ 1] classified cerebral edema into cytotoxic and vasogenic types. The cerebral edema associated with intracranial tumors is vasogenic in origin. Other than anecdotal references to the severity of edema associated with fast-growing metastatic tumors and gliomas, most textbooks on neuropathology and neurosurgery contain little information about the mechanisms o f its production. Granted, the ultimate event is the breakdown of the blood-brain barrier (BBB) with leakage of plasma, but what are the other factors involved? It appears that the growth rate of the tumor may be important. It is known that malignant gliomas alter the BBB more than slow-growing benign gliomas and hence, are associated with more edema. However, studies of the cell-cycle kinetics of meningiomas or other tumors are needed to relate their growth characteristics with the amount of associated cerebral edema. The size of the tumor may be important in some cases. C a n large tumors cause cerebral edema solely by their size, even if their growth rate is slow? An analogy can be drawn here with subdural hematomas. Chronic subdural hematomas, presumably caused by repeated small episodes of rebleeding, can grow larger than acute subdural hematomas and yet can be associated with less edema than the latter. Again, a need to put together growth characteristics and size is evident. Do tumors secrete edemogenic substances? N o firm evidence is available to support this hypothesis, other than one paper cited by Maiuri et al that suggests such a mechanism.
Do tumor metabolites such as necrotic cells, polyamines, and D N A cause cerebral edema? Such possibilities exist with intraaxial tumors, but are unlikely to operate in noninvasive meningiomas. It has been suggested that some meningiomas, and perhaps other tumors, cause cerebral edema by compression of superficial veins and/or venous sinuses. One can only surmise that this happens in a few cases. Angiographic studies of tumors that are likely to compress veins may shed more light on this issue. Those interested in central nervous system neoplasia should be aware that cerebral edema associated with intracranial tumors may be multifactorial. The cause of edema in one patient may be different from that of another. Much work needs to be done, especially because improvements in the drug treatment of cerebral edema may depend on such studies. In the lung and the brain, edema can kill or seriously damage the patient. There is evidence that myelin sheaths may break down due to chronic edema. Herniation phenomena are clinically dangerous. Preoperative morbidity, operative difficulties and slow or incomplete postoperative recovery can all be traced to this complication. Cerebral edema associated with meningiomas in particular, and intracranial tumors in general, needs more scientific investigation. VENKATA R. CHALLA, M.D. Winston-Salem, North Carolina
Reference I. Klatzo 1. Neuropathological aspects of brain edema. J Neuropathol Exp Neurol 1967;26:1-14.