AJDRAJNR - American Journal of Neuroradiology

This Article
Right arrow Abstract Freely available
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via CrossRef
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Forbes, K. P.N.
Right arrow Articles by Heiserman, J. E.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Forbes, K. P.N.
Right arrow Articles by Heiserman, J. E.

Evidence for Cytotoxic Edema in the Pathogenesis of Cerebral Venous Infarction

Kirsten P.N. Forbesa, James G. Pipea and Joseph E. HeisermanGo,a

a From the Division of Neuroradiology (K.P.N.F., J.E.H.) and MRI Department (J.G.P.), Barrow Neurological Institute, St. Joseph's Hospital and Medical Center, Phoenix, AZ.



View larger version (52K):

[in a new window]
 
FIG 1. Subject 6. A, T1-weighted image (450/14/1) showing slightly swollen right frontal cortex and no signal change.

B, T2-weighted image (2050/91/1) depicting a ring of signal hyperintensity in right frontal cortex.

C, Isotropic diffusion-weighted image revealing a more hyperintense right frontal cortex than B.

D, ADC showing corresponding decrease suggesting cytotoxic edema.



View larger version (15K):

[in a new window]
 
FIG 2. This graph shows the relationship between log of the ratio of the ADC value in CVI compared with normal brain and symptom duration. A log plot was performed as data appeared to show an exponential relationship with time. Subjects scanned within 2 days of symptom onset show a reduction in ADC within CVI, suggesting cytotoxic edema. By 4 to 6 days, CVI shows a similar ADC to that of normal brain. By 11 days, ADC is higher in CVI than in normal brain, suggesting vasogenic edema. The numbers adjacent to each point indicate the subject identification (see Table). Follow-up results are available for subject 8 (open square symbol). Subjects who underwent a single study are identified by a closed black circle. Error bars indicate the SD of signal intensity.FIG 3. This graph shows the relationship between percent T2 signal change and symptom duration. For each subject, the T2 signal within CVI has been compared with normal brain and the percent change in T2 signal calculated. Signal intensity of CVI appears to peak around day 2. The numbers adjacent to each point indicate the subject identification (Table). Follow-up results are available for subject 8 (open square symbol). Subjects who underwent a single study are indicated by a closed black circle. Error bars indicate the SD of signal intensity



View larger version (176K):

[in a new window]
 
FIG 4. Subject 8. A, MR venography (day 2) showing no flow in the internal cerebral veins, straight sinus, or vein of Galen.

B, T1-weighted image (450/14/1) (day 2) revealing swollen hypointense thalami.

C, T2-weighted image (2050/91/1) (day 2) depicting swollen hyperintense thalami.

D, Isotropic diffusion-weighted image (6500/101/1) (day 2) showing mixed hyperintense and isointense thalami.

E, Isotropic ADC map (day 2) depicting hypointense thalamic core (suggesting cytotoxic edema) with hyperintense rim (suggesting vasogenic edema).

F, T2-weighted image (2050/91/1) (day 6) revealing less swollen but still hyperintense thalami.

G, Diffusion-weighted image (6500/101/1) (day 6) is unchanged from that of day 2.

H, ADC (day 6) showing decreased signal intensity of rim, suggesting resolving vasogenic edema.

I, T2-weighted image (2050/91/1) (day 11) depicting decrease in thalamic swelling and hyperintensity.

J, Diffusion-weighted image (6500/101/1) (day 11) showing decreased volume of signal change.

K, ADC (day 11) is normal.