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Brain edema
Vasogenic edema
Brain edema may result from a wide array of causes,
which can be divided into the four principal forms listed
in Table–3 Clinically, multiple forms of brain
edema can occur simultaneously, and often the predominating form depends on the inciting cause as well as
the time course of the disease. Whether intracellular
or extracellular, edema appears mildly to moderately
hypoattenuating to normal brain parenchyma on CT
images and T1 hypointense and T2 hyperintense on MR
images. Because edema fluid is distributed within a
microenvironment of cells and macromolecules, it will
also appear hyperintense on FLAIR and other pure
water‐nulling sequences.
Vasogenic edema occurs because of a disruption of
the tight junctions of the blood–brain barrier, resulting
in extravasation of high‐protein fluid into the brain.
Vasogenic edema is extracellular, so it tends to preferentially accumulate in white matter, which has a sparser
cellular density and therefore more potential space for
fluid distribution compared to highly cellular gray matter.3 Depending on the initiating cause and volume of
fluid, edema can distribute widely (Figures 2.2.2, 2.2.3).
Cytotoxic edema
Cytotoxic edema occurs as a result of ischemia resulting
in cell membrane Na/K pump dysfunction, increased
intracellular fluid volume, and cell swelling. Because
of the underlying cause and the intracellular nature of
this form of edema, white and gray matter may both be
affected, and the distribution of edema roughly ­conforms
to the geographic distribution of ischemia (Figure 2.2.1).3
In most instances, cytotoxic edema occurs in combination with vasogenic edema. Diffusion‐weighted imaging
has been used to discriminate between the two forms
following acute episodes of ischemia, with reduced
apparent diffusion coefficient (ADC) intensity reflecting
predominantly cytotoxic edema.4
Interstitial or hydrocephalic edema
Interstitial edema most often occurs in association with
obstructive hydrocephalus when intraventricular pressure increases, causing transependymal CSF migration
into adjacent brain parenchyma. As a result, hydrostatic
edema preferentially occurs within periventricular
parenchyma and is extracellular (Figure 2.2.4). Unlike
vasogenic edema, interstitial edema fluid is a transudate
containing little in the way of cells or macromolecules.3
Osmotic edema
Osmotic edema occurs rarely and is caused by reduced
plasma osmolality resulting from water intoxication,
hemodialysis, or metabolic disorders that reduce plasma
sodium or glucose concentration. The imbalance in
brain extracellular fluid osmolality and plasma osmolality results in a fluid shift to the brain leading to ­formation
of extracellular edema.3
Atlas of Small Animal CT and MRI, First Edition. Erik R. Wisner and Allison L. Zwingenberger.
© 2015 John Wiley & Sons, Inc. Published 2015 by John Wiley & Sons, Inc.
Brain Edema
Table 2.2.1 Distribution and causes of brain edema.
Intracellular gray and white
Extracellular predominately
white matter
Extracellular periventricular
Cell membrane Na/K pump
dysfunction due to cell
hypoxia from ischemia
Disruption of blood–brain barrier
resulting in extravasation of
high‐protein fluid
Increased intraventricular
pressure. Usually from
obstructive hydrocephalus
Systemic plasma
Figure 2.2.1 Cytotoxic Edema (Canine)
(a) T1, TP
(b) FL, TP
(c) T2, DP
3y FS Dachshund with right‐sided cerebellar infarction. There is a well‐circumscribed geographic region of FLAIR and T2 hyperintensity
involving the right cerebellum (b,c: arrow). The T2 hyperintensity is due, in part, to intracellular cytotoxic edema resulting from cell
hypoxia. The lesion distribution coincides with the tissue volume normally perfused by the right rostral cerebellar artery.
Figure 2.2.2 Vasogenic Edema (Canine)
3y MC Basset Hound with aspergillosis involving the frontal sinus and forebrain. This
­unenhanced CT image is caudal to the primary lesion. Marked, diffuse hypoattenuation is
evident involving the white matter of the right cerebral hemisphere because of the ­presence
of vasogenic edema. Although edema is recognized on CT images, it may be less ­conspicuous
than on corresponding MR images.
(a) CT, TP
164 Atlas of Small Animal CT and MRI
Figure 2.2.3 Vasogenic Edema (Canine)
Adult dog of unknown age and gender with a large left frontal lobe meningioma. This
image is at a level caudal to the mass. Marked, diffuse hyperintensity is evident involving
the white m
­ atter of the left cerebral hemisphere, representing vasogenic edema. There is
also diffuse volume expansion of the white matter associated with prominent right‐sided
midline shift.
(a) FL, TP
Figure 2.2.4 Interstitial Edema (Canine)
(a) T1+C, DP
(b) T1, TP
(c) FL, TP
6y FS Toy Poodle with a caudal fossa meningioma causing obstruction of the ventricular system (a). Images b and c are at the level of
the rostral horns of the lateral ventricles. The thin, hyperintense rim surrounding the rostral horns of the lateral ventricles on the FLAIR
image (c: arrowheads) represents transependymal migration of cerebrospinal fluid to the periventricular extracellular fluid space due to
increased intraventricular hydrostatic pressure.
1. Betz AL, Iannotti F, Hoff JT. Brain edema: a classification based
on blood–brain barrier integrity. Cerebrovasc Brain Metab Rev.
2. Iencean SM. Brain edema – a new classification. Med Hypotheses.
3. Nag S, Manias JL, Stewart DJ. Pathology and new players in the
pathogenesis of brain edema. Acta Neuropathol. 2009;118:
4. Loubinoux I, Volk A, Borredon J, Guirimand S, Tiffon B, Seylaz J,
et al. Spreading of vasogenic edema and cytotoxic edema assessed
by quantitative diffusion and T2 magnetic resonance imaging.
Stroke. 1997;28:419–426; discussion 426–417.