Contribution of vasogenic and cellular edema to traumatic brain swelling measured by diffusion-weighted imaging

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✓ The contribution of brain edema to brain swelling in cases of traumatic brain injury remains a critical problem. The authors believe that cellular edema, the result of complex neurotoxic events, is the major contributor to brain swelling and that vasogenic edema, secondary to blood-brain barrier compromise, may be overemphasized. The objective of this study, therefore, was to quantify temporal water content changes and document the type of edema that forms during the acute and late stages of edema development following closed head injury (CHI). The measurement of brain water content was based on magnetic resonance imaging—determined values of tissue longitudinal relaxation time (T1-weighted imaging) and their subsequent conversion to percentage of water, whereas the differentiation of edema formation (cellular vs. vasogenic) was based on the measurement of the apparent diffusion coefficient (ADC) by diffusion-weighted imaging.

A new impact-acceleration model was used to induce CHI. Thirty-six adult Sprague—Dawley rats were separated into two groups: Group I, control (six animals); and Group II, trauma (30 animals). Fast ADC measurements (localized, single-voxel) were obtained sequentially (every minute) up to 1 hour postinjury. The T1-weighted images, used for water content determination, and the diffusion-weighted images (ADC measurement with conventional diffusion-weighted imaging) were obtained at the end of the 1st hour postinjury and on Days 1, 3, 7, 14, 28, and 42 in animals from the trauma and control groups.

In the animals subjected to trauma, the authors found a significant increase in ADC (10 ± 5%) and brain water content (1.3 ± 0.9%) during the first 60 minutes postinjury. This is consistent with an increase in the volume of extracellular fluid and vasogenic edema formation as a result of blood-brain barrier compromise. This transient increase, however, was followed by a continuing decrease in ADC that began 40 to 60 minutes postinjury and reached a minimum value on Days 7 to 14 (10 ± 3% reduction). Because the water content of the brain continued to increase during the first 24 hours postinjury (1.9 ± 0.9%), it is suggested that the decreased ADC indicated cellular edema formation, which started to develop soon after injury and became dominant between 1 and 2 weeks postinjury.

The study provides supportive evidence that cellular edema is the major contributor to posttraumatic swelling in diffuse CHI and defines the onset and duration of the increase in cellular volume.

Article Information

Address reprint requests to: Anthony Marmarou, Ph.D., Division of Neurosurgery, P.O. Box 508, Medical College of Virginia Station, Sanger Hall, Room 8004, 1101 East Marshall Street, Richmond, Virginia 23298.

© AANS, except where prohibited by US copyright law.

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Figures

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    Bar graphs showing the time course of water content in the whole brain (upper left and right), in the cortex (lower left), and in the caudate nucleus (lower right). Upper Left: In the control group, water content did not change during the 6-week period in any region or in the whole brain. Upper Right: In the trauma group, water content immediately increased after trauma, reaching its maximum value at the end of the 1st day. During the next 2 weeks water content was significantly higher than control values except on Day 3 when a transient decrease was observed. Lower Left and Right: In the trauma group, brain swelling was diffuse, that is, the water map did not show any regional difference in water content. The maximum water content was observed 24 hours posttrauma. The reduction in water content observed on Day 3 was consistent in the caudate nucleus, cortex, and whole brain. The subsequent increase in water content may signify a second BBB opening although the ADC remained low.

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    Line graphs displaying the time course of ADCs in the whole brain. Upper: In the control group, the ADC did not change during the 6-week period in any of the regions or in the whole brain. Lower: In the trauma group, during the first 45 minutes posttrauma the ADC showed a significant increase. This transient elevation was followed by a gradual decrease beginning 40 to 60 minutes postinjury, and the ADC crossed the baseline value at 24 hours. Beyond this time the ADC reduction continued and its minimum was observed at 7 to 14 days postinjury.

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    Scatterplots showing changes in ventricular size during the acute swelling process. Upper: In the control group, the ventricular size measured by MR imaging remained the same during the 6 weeks and did not show any significant change. Lower: In the trauma group, the ventricular size changed during the 6-week period following head injury. It was smallest at 1 hour posttrauma and largest at 3 days and 6 weeks postinjury.

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