Mechanisms of Tumor-related Brain Edema
Mechanisms of Tumor-related Brain Edema
Cerebral edema contributes strongly to symptoms associated with brain tumors. Although the introduction of corticosteroids has greatly simplified treatment of patients with newly diagnosed tumors, these drugs are associated with marked side effects during the long-term treatment that is often necessary in the recurrences. Therefore, a better understanding of mechanisms related to the evolution and clearance of tumor-related edema with the aid of modern imaging and molecular methodology is clearly necessary. Recently, researchers have focused on molecular mechanisms of edema development and have demonstrated alternative routes—such as the inhibition of vascular endothelial growth factor receptor inhibitors—to be explored for treating edema. In this review the author focuses on established and current concepts regarding the pathophysiology of cerebral edema and its treatment.
Edema associated with brain tumors plays a major role in determining symptoms caused by cerebral tumors. Not only does edema cause additional mass effect, often exceeding the mass induced by the tumor itself and resulting in increased intracranial pressure, it also leads to neurological disturbances by disrupting tissue homeostasis and reducing local blood flow. Near ly all focal lesions, including primary and metastatic tumors, abscesses, encephalitides, and radionecroses, pro- duce vasogenic edema. Although steroids have facilitated the management of edema in patients with newly diagnosed brain tumors, long-term therapy of tumor-associated edema remains an important issue in the context of recurrent malignant gliomas or lesions treated using radiosurgery or radiotherapy rather than resection. Nevertheless, authors of only a few studies have specifically ad dressed clinical management issues of cerebral edema. Furthermore, viewing tumor-associated edema as a single entity is probably not justified. For example, in contrast to edema surrounding metastases (Fig. 1) or meningiomas, peritumoral edema associated with high-grade gliomas (Fig. 2) is characterized by extensive infiltration of tumor cells. Types of peritumoral edema may therefore be distinguishable, depending on histopathological and clinical prop erties. Adopting a more differentiated view would likely lead to improved strategies of treatment and diagnosis for brain tumors accompanied by peritumoral edema.
(Enlarge Image)
(Enlarge Image)
In this review I summarize the established and new concepts regarding the pathophysiology of peritumoral edema based on morphological and molecular findings, as well as modern imaging.
Cerebral edema contributes strongly to symptoms associated with brain tumors. Although the introduction of corticosteroids has greatly simplified treatment of patients with newly diagnosed tumors, these drugs are associated with marked side effects during the long-term treatment that is often necessary in the recurrences. Therefore, a better understanding of mechanisms related to the evolution and clearance of tumor-related edema with the aid of modern imaging and molecular methodology is clearly necessary. Recently, researchers have focused on molecular mechanisms of edema development and have demonstrated alternative routes—such as the inhibition of vascular endothelial growth factor receptor inhibitors—to be explored for treating edema. In this review the author focuses on established and current concepts regarding the pathophysiology of cerebral edema and its treatment.
Edema associated with brain tumors plays a major role in determining symptoms caused by cerebral tumors. Not only does edema cause additional mass effect, often exceeding the mass induced by the tumor itself and resulting in increased intracranial pressure, it also leads to neurological disturbances by disrupting tissue homeostasis and reducing local blood flow. Near ly all focal lesions, including primary and metastatic tumors, abscesses, encephalitides, and radionecroses, pro- duce vasogenic edema. Although steroids have facilitated the management of edema in patients with newly diagnosed brain tumors, long-term therapy of tumor-associated edema remains an important issue in the context of recurrent malignant gliomas or lesions treated using radiosurgery or radiotherapy rather than resection. Nevertheless, authors of only a few studies have specifically ad dressed clinical management issues of cerebral edema. Furthermore, viewing tumor-associated edema as a single entity is probably not justified. For example, in contrast to edema surrounding metastases (Fig. 1) or meningiomas, peritumoral edema associated with high-grade gliomas (Fig. 2) is characterized by extensive infiltration of tumor cells. Types of peritumoral edema may therefore be distinguishable, depending on histopathological and clinical prop erties. Adopting a more differentiated view would likely lead to improved strategies of treatment and diagnosis for brain tumors accompanied by peritumoral edema.
(Enlarge Image)
(Enlarge Image)
In this review I summarize the established and new concepts regarding the pathophysiology of peritumoral edema based on morphological and molecular findings, as well as modern imaging.
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