The concept of cerebral edema has been recognized for more than 2000 years, yet an understanding of the complex physiology of this condition has evolved only within the past 30 years. Ancient Greek authors used the term "oidzma" to describe the swelling of the brain that resulted from compound skull fractures. Hippocrates noted that removal of the overlying skull bones allowed the injured brain to swell outward, thus minimizing compression of normal tissue trapped within the cranial vault. The Monro-Kellie doctrine later recapitulated this concept, affirming that when ''water or other matter is effused or secreted from the blood vessels ... a quantity of blood equal in bulk to the effused matter, will be pressed out ofthe cranium.'' This indiscriminate concept of brain swelling was cited in a diverse range of clinical settings until 1967, when Igor Klatzo defined the modern classification of edema based on pathophysiology. Cerebral edema, according to Klatzo, was defined as ''an abnormal accumulation of fluid associated with volumetric enlargement of the brain.'' This entity was divided into vasogenic edema, characterized by derangement of the blood-brain barrier (BBB), and cytotoxic edema, related to intracellular swelling in the absence of changes at the BBB. The term cytotoxic edema has recently been reserved for states associated with toxin-induced cellular swelling. Klatzo emphasized that these two forms usually coexisted. In 1975, Robert Fishman added interstitial edema as a distinct entity by describing the transepen-dymal flow of cerebrospinal fluid (CSF) into the periventricular white matter in individuals with acute obstructive hydrocephalus; this form was later termed hydrocephalic edema. In similar fashion, ischemic

Encyclopedia of the Human Brain Volume 1

Copyright 2002, Elsevier Science (USA).

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Table I

Classification of Cerebral Edema




Blood-brain barrier


Clinical correlation



White matter

Disrupted Vascular permeability



White or gray matter Intact

Hydrocephalic Ischemic Hydrostatic Osmotic

Extracellular White matter Intact

Intra- and extracellular White and gray matter Disrupted

Extracellular White and gray matter Disrupted

Intra- and extracellular White and gray matter Intact

Cellular injury

Transependymal pressure Hypoxia

Hydrostatic pressure Osmotic pressure

Lead encephalopathy Neoplastic disease Infection

Fulminant hepatic failure Traumatic brain injury High-altitude cerebral edema Toxin exposure Ischemia

Traumatic brain injury Fulminant hepatic failure Reye's syndrome Hydrocephalus Ischemia

Hypertensive encephalopatby Hyponatremia Dialysis disequilibrium Diabetic ketoacidosis edema was described, incorporating elements of both cytotoxic and vasogenic forms. Additional classifications based on mechanism and location of excess fluid include hydrostatic edema and osmotic edema. Hydrostatic edema results from increased hydrostatic forces with associated disruption of the BBB, as occurs in the setting ofhypertensive encephalopathy. Osmotic edema has been ascribed to states of plasma hypoos-molarity that result in cellular swelling with preservation of the BBB. Table I summarizes the nomenclature of cerebral edema. This classification scheme emphasizes the predominant form of edema associated with several clinical scenarios and delineates the corresponding pathophysiology. The remainder of this article utilizes this classification of cerebral edema, emphasizing the role of each form in a variety of clinical encounters.

Consideration of the specific pathophysiologic mechanisms is crucial for establishing a fundamental approach to the various forms of cerebral edema. Each form of cerebral edema results in a net gain of water in the brain, although different mechanisms determine the specific location of water accumulation and resultant pathology. Numerous descriptions fail to distinguish cerebral edema from other causes of intracranial hypertension. Cerebral edema may result in intracranial hypertension, but the two conditions are not synonymous because intracranial hypertension may result from increased cerebral blood volume or increased CSF content. This review specifically focuses on cerebral edema, in distinction from other causes of intracranial hypertension. Various forms of cerebral edema may coexist and are often closely interrelated. One form of edema may also lead to the development of another, particularly in vasogenic and cytotoxic edema. For these reasons it is particularly important to consider the time course involved in specific clinical scenarios. The underlying processes must be delineated to understand and develop rational therapeutic approaches that focus on the particular pathophysiologic mechanism.

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