Published online November 1, 2002, 10.1148/rg.e7
(Radiographics. 2003;23:e7-e7.)
© RSNA, 2003
Imaging Tutorial: Differential Diagnosis of Bright Lesions on Diffusion-weighted MR Images1
Tadeusz W. Stadnik, MD, PhD,
Philippe Demaerel, MD, PhD,
Robert R Luypaert, PhD,
Christo Chaskis, MD,
Katrijn L. Van Rompaey, MD,
Alex Michotte, MD and
Michel J. Osteaux, MD, PhD
1 From the Departments of Radiology (T.W.S., R.R.L., M.J.O.), Neurosurgery (C.C., K.L.V.R.), and Neurology (A.M.), Academisch Ziekenhuis AZ Vrije Universiteit, Laarbeeklaan 101, 1090 Brussels, Belgium; and the Department of Radiology, Universitaire Ziekenhuizen, Leuven, Belgium (P.D.). Presented as a scientific exhibit at the 2001 RSNA scientific assembly. Received January 16, 2002, revision requested April 4, revision received and accepted August 18. Address correspondence to T.W.S. (e-mail: cradrew@az.vub.ac.be).
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Abstract
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High sensitivity (94%) and specificity (100%) have been reported in the diagnosis of acute cerebral infarction with diffusion-weighted magnetic resonance (MR) imaging. However, high signal intensity on diffusion-weighted MR images and low apparent diffusion coefficient values (similar to the findings in acute cerebral infarction) were reported in such diverse conditions as hemorrhage, abscess, lymphoma, and even Creutzfeldt-Jakob disease. The differential diagnosis of these conditions (eg, acute ischemic infarction and acute cerebral hemorrhage) is critical for the determination of appropriate treatment. The authors present a systematic review of bright lesions on diffusion-weighted MR images and their differential diagnosis, with emphasis on the practical and clinical approaches of differential diagnosis.
© RSNA, 2002
Index Terms: Brain, abscess, 13.256 • Brain, diseases, 13.836, 13.871 • Brain, ischemia, 13.781, 13.782 • Brain, MR, 13.12144 • Brain neoplasms, diagnosis, 13.12144 • Brain neoplasms, primary, 13.36 • Brain neoplasms, secondary, 13.38 • Encephalitis, 13.253 • Magnetic resonance (MR), diffusion study, 13.12144
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Basic Physics of Diffusion-weighted (DW) Magnetic Resonance (MR) Imaging
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This topic was covered in an article titled Diffusion imaging: from basic physics to practical imaging, published in RSNA EJ/RadioGraphics in 1999.
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Acute Infarction
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Typical Presentation on DW Images and Apparent Diffusion Coefficient (ADC) Maps
Acute ischemic lesions are characterized by high signal intensity on DW images and low ADC values. The widely accepted explanation is that the interruption of cerebral blood flow results in rapid (within minutes) breakdown of energy metabolism and ion exchange pumps. This leads to a massive shift of water from the extracellular into the intracellular compartment (cytotoxic edema) and produces a typical "bright spot" on DW MR images (1) (Figs 1, 2).
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Figure 1a. Acute infarction within the 1st hour after stroke. (a) Fast T2-weighted spin-echo (SE) image. (b, c) DW (trace) multishot echo-planar image (b) and corresponding ADC map (c). (d, e) Perfusion-weighted multishot echo-planar imaging; (d) relative cerebral blood volume and (e) time-to-peak maps calculated from the time-intensity curve after injection of 40 mL of gadopentetate dimeglumine. (f) Time-of-flight (TOF) MR angiogram. Comments: Acute thrombosis of the right middle cerebral artery. On T2-weighted SE image, only scattered white matter hyperintensities are seen. Small occipital hyperintensity is seen on DW image, with moderate decrease in the ADC value (0.48 x 10-3 mm2/sec). There is an important perfusion deficit ("penumbra" [2]) in the middle cerebral artery territory.
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Figure 1b. Acute infarction within the 1st hour after stroke. (a) Fast T2-weighted spin-echo (SE) image. (b, c) DW (trace) multishot echo-planar image (b) and corresponding ADC map (c). (d, e) Perfusion-weighted multishot echo-planar imaging; (d) relative cerebral blood volume and (e) time-to-peak maps calculated from the time-intensity curve after injection of 40 mL of gadopentetate dimeglumine. (f) Time-of-flight (TOF) MR angiogram. Comments: Acute thrombosis of the right middle cerebral artery. On T2-weighted SE image, only scattered white matter hyperintensities are seen. Small occipital hyperintensity is seen on DW image, with moderate decrease in the ADC value (0.48 x 10-3 mm2/sec). There is an important perfusion deficit ("penumbra" [2]) in the middle cerebral artery territory.
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Figure 1c. Acute infarction within the 1st hour after stroke. (a) Fast T2-weighted spin-echo (SE) image. (b, c) DW (trace) multishot echo-planar image (b) and corresponding ADC map (c). (d, e) Perfusion-weighted multishot echo-planar imaging; (d) relative cerebral blood volume and (e) time-to-peak maps calculated from the time-intensity curve after injection of 40 mL of gadopentetate dimeglumine. (f) Time-of-flight (TOF) MR angiogram. Comments: Acute thrombosis of the right middle cerebral artery. On T2-weighted SE image, only scattered white matter hyperintensities are seen. Small occipital hyperintensity is seen on DW image, with moderate decrease in the ADC value (0.48 x 10-3 mm2/sec). There is an important perfusion deficit ("penumbra" [2]) in the middle cerebral artery territory.
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Figure 1d. Acute infarction within the 1st hour after stroke. (a) Fast T2-weighted spin-echo (SE) image. (b, c) DW (trace) multishot echo-planar image (b) and corresponding ADC map (c). (d, e) Perfusion-weighted multishot echo-planar imaging; (d) relative cerebral blood volume and (e) time-to-peak maps calculated from the time-intensity curve after injection of 40 mL of gadopentetate dimeglumine. (f) Time-of-flight (TOF) MR angiogram. Comments: Acute thrombosis of the right middle cerebral artery. On T2-weighted SE image, only scattered white matter hyperintensities are seen. Small occipital hyperintensity is seen on DW image, with moderate decrease in the ADC value (0.48 x 10-3 mm2/sec). There is an important perfusion deficit ("penumbra" [2]) in the middle cerebral artery territory.
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Figure 1e. Acute infarction within the 1st hour after stroke. (a) Fast T2-weighted spin-echo (SE) image. (b, c) DW (trace) multishot echo-planar image (b) and corresponding ADC map (c). (d, e) Perfusion-weighted multishot echo-planar imaging; (d) relative cerebral blood volume and (e) time-to-peak maps calculated from the time-intensity curve after injection of 40 mL of gadopentetate dimeglumine. (f) Time-of-flight (TOF) MR angiogram. Comments: Acute thrombosis of the right middle cerebral artery. On T2-weighted SE image, only scattered white matter hyperintensities are seen. Small occipital hyperintensity is seen on DW image, with moderate decrease in the ADC value (0.48 x 10-3 mm2/sec). There is an important perfusion deficit ("penumbra" [2]) in the middle cerebral artery territory.
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Figure 1f. Acute infarction within the 1st hour after stroke. (a) Fast T2-weighted spin-echo (SE) image. (b, c) DW (trace) multishot echo-planar image (b) and corresponding ADC map (c). (d, e) Perfusion-weighted multishot echo-planar imaging; (d) relative cerebral blood volume and (e) time-to-peak maps calculated from the time-intensity curve after injection of 40 mL of gadopentetate dimeglumine. (f) Time-of-flight (TOF) MR angiogram. Comments: Acute thrombosis of the right middle cerebral artery. On T2-weighted SE image, only scattered white matter hyperintensities are seen. Small occipital hyperintensity is seen on DW image, with moderate decrease in the ADC value (0.48 x 10-3 mm2/sec). There is an important perfusion deficit ("penumbra" [2]) in the middle cerebral artery territory.
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Figure 2a. Acute infarction within the first 6 hours after stroke. (a) Fast T2-weighted SE image. (b, c) DW (trace) multishot echo-planar image and corresponding ADC map. (d, e) Perfusion-weighted multishot echo-planar imaging; (d) relative cerebral blood volume and (e) time-to-peak maps calculated from the time-intensity curve after injection of 40 mL of gadopentetate dimeglumine (f) TOF MR angiogram. Comment: Acute thrombosis of the left carotid artery. On T2-weighted SE image, only a faint increase in signal intensity in the insular cortex is seen. There is typical hyperintensity on DW image, with a decreased ADC value. There is an important perfusion deficit and only a limited penumbra (2).
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Figure 2b. Acute infarction within the first 6 hours after stroke. (a) Fast T2-weighted SE image. (b, c) DW (trace) multishot echo-planar image and corresponding ADC map. (d, e) Perfusion-weighted multishot echo-planar imaging; (d) relative cerebral blood volume and (e) time-to-peak maps calculated from the time-intensity curve after injection of 40 mL of gadopentetate dimeglumine (f) TOF MR angiogram. Comment: Acute thrombosis of the left carotid artery. On T2-weighted SE image, only a faint increase in signal intensity in the insular cortex is seen. There is typical hyperintensity on DW image, with a decreased ADC value. There is an important perfusion deficit and only a limited penumbra (2).
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Figure 2c. Acute infarction within the first 6 hours after stroke. (a) Fast T2-weighted SE image. (b, c) DW (trace) multishot echo-planar image and corresponding ADC map. (d, e) Perfusion-weighted multishot echo-planar imaging; (d) relative cerebral blood volume and (e) time-to-peak maps calculated from the time-intensity curve after injection of 40 mL of gadopentetate dimeglumine (f) TOF MR angiogram. Comment: Acute thrombosis of the left carotid artery. On T2-weighted SE image, only a faint increase in signal intensity in the insular cortex is seen. There is typical hyperintensity on DW image, with a decreased ADC value. There is an important perfusion deficit and only a limited penumbra (2).
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Figure 2d. Acute infarction within the first 6 hours after stroke. (a) Fast T2-weighted SE image. (b, c) DW (trace) multishot echo-planar image and corresponding ADC map. (d, e) Perfusion-weighted multishot echo-planar imaging; (d) relative cerebral blood volume and (e) time-to-peak maps calculated from the time-intensity curve after injection of 40 mL of gadopentetate dimeglumine (f) TOF MR angiogram. Comment: Acute thrombosis of the left carotid artery. On T2-weighted SE image, only a faint increase in signal intensity in the insular cortex is seen. There is typical hyperintensity on DW image, with a decreased ADC value. There is an important perfusion deficit and only a limited penumbra (2).
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Figure 2e. Acute infarction within the first 6 hours after stroke. (a) Fast T2-weighted SE image. (b, c) DW (trace) multishot echo-planar image and corresponding ADC map. (d, e) Perfusion-weighted multishot echo-planar imaging; (d) relative cerebral blood volume and (e) time-to-peak maps calculated from the time-intensity curve after injection of 40 mL of gadopentetate dimeglumine (f) TOF MR angiogram. Comment: Acute thrombosis of the left carotid artery. On T2-weighted SE image, only a faint increase in signal intensity in the insular cortex is seen. There is typical hyperintensity on DW image, with a decreased ADC value. There is an important perfusion deficit and only a limited penumbra (2).
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Figure 2f. Acute infarction within the first 6 hours after stroke. (a) Fast T2-weighted SE image. (b, c) DW (trace) multishot echo-planar image and corresponding ADC map. (d, e) Perfusion-weighted multishot echo-planar imaging; (d) relative cerebral blood volume and (e) time-to-peak maps calculated from the time-intensity curve after injection of 40 mL of gadopentetate dimeglumine (f) TOF MR angiogram. Comment: Acute thrombosis of the left carotid artery. On T2-weighted SE image, only a faint increase in signal intensity in the insular cortex is seen. There is typical hyperintensity on DW image, with a decreased ADC value. There is an important perfusion deficit and only a limited penumbra (2).
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Differential Diagnosis with Venous Stroke
Differential diagnosis of arterial and venous stroke may be impossible with use of acute-stroke MR imaging protocols (ie, T2-weighted SE, fluid-attenuated inversion recovery [FLAIR], DW or perfusion-weighted imaging, or MR arteriography). Venous stroke may be characterized by high signal intensity on DW images and a low ADC value (Fig 3). (For more information, see the section on Venous Infarction.) Important perfusion abnormalities have also been reported in venous stroke (16,17), and normal findings at MR arteriography do not exclude arterial stroke (eg, small branches or early spontaneous recanalization).
Hints for differential diagnosis:
- Clinical presentation (typically acute onset in arterial stroke; in venous sinus thrombosis, more insidious, frequently beginning with severe headache and/or seizures).
- Early hemorrhage, especially when close to the venous sinuses (unusual in acute ischemic stroke).
- With either or both of the above, perform MR or computed tomography (CT) venography
Differential Diagnosis with Cerebritis
The differential diagnosis of early-stage cerebral abscesses (cerebritis) (Fig 4) and acute infarction may be potentially problematic on conventional MR images or DW images. However, to our knowledge, only the early capsule stages of cerebral abscesses have been reported (53,54,58) on DW images.
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Figure 4a. Early stage of cerebral abscess. (a) T2-weighted SE image, (b) contrast-enhanced T1-weighted SE image, and (c, d) DW echo-planar image (c) and corresponding ADC map (d). The signal intensity on the DW image and ADC map looks like that of an acute stroke. However, on the T2-weighted and enhanced T1-weighted images a fine capsule is readily recognized.
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Figure 4b. Early stage of cerebral abscess. (a) T2-weighted SE image, (b) contrast-enhanced T1-weighted SE image, and (c, d) DW echo-planar image (c) and corresponding ADC map (d). The signal intensity on the DW image and ADC map looks like that of an acute stroke. However, on the T2-weighted and enhanced T1-weighted images a fine capsule is readily recognized.
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Figure 4c. Early stage of cerebral abscess. (a) T2-weighted SE image, (b) contrast-enhanced T1-weighted SE image, and (c, d) DW echo-planar image (c) and corresponding ADC map (d). The signal intensity on the DW image and ADC map looks like that of an acute stroke. However, on the T2-weighted and enhanced T1-weighted images a fine capsule is readily recognized.
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Figure 4d. Early stage of cerebral abscess. (a) T2-weighted SE image, (b) contrast-enhanced T1-weighted SE image, and (c, d) DW echo-planar image (c) and corresponding ADC map (d). The signal intensity on the DW image and ADC map looks like that of an acute stroke. However, on the T2-weighted and enhanced T1-weighted images a fine capsule is readily recognized.
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Hints for differential diagnosis:
- See the section on Inflammation: Abscess.
Background and Discussion
What Is the Evolution of Acute Stroke on DW Images and ADC Maps?
DW images.—The signal intensity of acute stroke on DW images increases during the 1st week after symptom onset and decreases thereafter; however, it remains hyperintense for a long period (up to 72 days in the study by Lansberg et al [3]). This pattern is most likely the result of two factors: initially to reduced diffusion and thereafter to increasing T2 (T2 "shine-through"). Because the DW imaging signal remains hyperintense for a long period, it is not ideal for estimating lesion age.
ADC values.—It is accepted that ADC values decline rapidly after the onset of ischemia and subsequently increase with the "flip-flop" from dark to bright 7-10 days later (4–8). This property may be used to differentiate the lesions older than 10 days from more acute ones (Table 1).
How Fast after Onset of Stroke Are Changes on DW Images and ADC Maps Detectable?
DW images and ADC maps show changes in ischemic brain tissue within hours after symptom onset, when no abnormalities are typically seen on conventional MR images (1,2,4–7,9,10).
Presumed CausesAcute ischemic lesions are characterized by high signal intensity on DW images and a low ADC (1). The ADC is believed to be low because of a shift of water within hypoxic brain parenchyma, from the extracellular to the intracellular compartment, where water diffusion is relatively restricted (1).
What are the Sensitivity and Specificity of DW images and ADC Maps in Acute Stroke?
The majority of studies report high sensitivity and specificity for DW images and ADC maps in the diagnosis of acute stroke (94%sensitivity and 100%specificity in the study by Lövblad et al [11] within the first 6 hours after stroke; 100%sensitivity and 100%specificity in the study by Gonzalez et al [12] in patients imaged within 6 hours of stroke symptom onset). In the study by Gonzalez et al (12), DW images indicated stroke in 14 patients, all of whom had a final diagnosis of acute stroke, and DW images were negative in eight patients, all of whom had a final clinical diagnosis other than stroke. On the other hand, there have been occasional reports of patients progressing to complete stroke after an initial negative DW imaging finding (13,14). The potential mechanism that may explain the lack of diffusion changes in the acute phase in these patients is that cerebral blood flow was at an intermediate level below the threshold for neuronal dysfunction (symptom onset) but above that of reduced diffusion (1).
Conclusions
The signal intensity of acute stroke on DW images increases during the 1st week after symptom onset and decreases thereafter, but signal remains hyperintense for a long period. The ADC values decline rapidly after the onset of ischemia and subsequently increase with the "flip-flop" from dark to bright 7-10 days later. This property may be used to differentiate the lesions older than 10 days from more acute ones. Most studies report high sensitivity and specificity for DW images and ADC maps in the diagnosis of acute stroke. There have been only occasional reports of patients progressing to complete stroke after an initial negative DW imaging finding. The differential diagnosis of arterial and venous stroke may be impossible with acute-stroke MR protocols (ie, including T2-weighted SE, FLAIR, DW and perfusion-weighted imaging, and MR arteriography). The clinical presentation and early hemorrhage, especially when near the venous sinuses, should prompt performance of MR or CT venography.
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Venous Infarction
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Typical Presentation on DW Images and ADC Maps
Diffusion findings in human venous infarction have so far been limited to conflicting case reports. The initial reports suggested increased to slightly decreased ADC values with hypo- to isointensity on DW images (15,16). These findings were explained by the presence of prominent vasogenic edema associated with mild cytotoxic edema. More recently, a larger series of venous infarctions with high signal intensity on DW images and low ADC values were reported (17–19). The findings were attributed to cytotoxic edema (Figs 5, 6).
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Figure 5a. Acute venous infarction (superior sagittal sinus thrombosis) with high signal intensity on DW images and low ADC values. (a) Transverse T2-weighted fast SE image (5500/128 [repetition time/echo time]; 6-mm section thickness; three signals averaged; echo train length, 23; and 230 x 512 matrix). (b) Transverse T1-weighted SE image (550/14), 6-mm section thickness, three signals averaged, one echo, and 192 x 256). (c, d) Transverse DW image (x = sensitizing direction) (c) multishot echo-planar image (800/123, one signal acquired, 6-mm section thickness) and corresponding ADC map (d). (e) Maximum-intensity projection of TOF venogram. These findings may be consistent with prominent cytotoxic edema. The differential diagnosis of hyperacute arterial stroke and venous stroke remains difficult on T2- or T1-weighed SE and DW images.
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Figure 5b. Acute venous infarction (superior sagittal sinus thrombosis) with high signal intensity on DW images and low ADC values. (a) Transverse T2-weighted fast SE image (5500/128 [repetition time/echo time]; 6-mm section thickness; three signals averaged; echo train length, 23; and 230 x 512 matrix). (b) Transverse T1-weighted SE image (550/14), 6-mm section thickness, three signals averaged, one echo, and 192 x 256). (c, d) Transverse DW image (x = sensitizing direction) (c) multishot echo-planar image (800/123, one signal acquired, 6-mm section thickness) and corresponding ADC map (d). (e) Maximum-intensity projection of TOF venogram. These findings may be consistent with prominent cytotoxic edema. The differential diagnosis of hyperacute arterial stroke and venous stroke remains difficult on T2- or T1-weighed SE and DW images.
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Figure 5c. Acute venous infarction (superior sagittal sinus thrombosis) with high signal intensity on DW images and low ADC values. (a) Transverse T2-weighted fast SE image (5500/128 [repetition time/echo time]; 6-mm section thickness; three signals averaged; echo train length, 23; and 230 x 512 matrix). (b) Transverse T1-weighted SE image (550/14), 6-mm section thickness, three signals averaged, one echo, and 192 x 256). (c, d) Transverse DW image (x = sensitizing direction) (c) multishot echo-planar image (800/123, one signal acquired, 6-mm section thickness) and corresponding ADC map (d). (e) Maximum-intensity projection of TOF venogram. These findings may be consistent with prominent cytotoxic edema. The differential diagnosis of hyperacute arterial stroke and venous stroke remains difficult on T2- or T1-weighed SE and DW images.
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Figure 5d. Acute venous infarction (superior sagittal sinus thrombosis) with high signal intensity on DW images and low ADC values. (a) Transverse T2-weighted fast SE image (5500/128 [repetition time/echo time]; 6-mm section thickness; three signals averaged; echo train length, 23; and 230 x 512 matrix). (b) Transverse T1-weighted SE image (550/14), 6-mm section thickness, three signals averaged, one echo, and 192 x 256). (c, d) Transverse DW image (x = sensitizing direction) (c) multishot echo-planar image (800/123, one signal acquired, 6-mm section thickness) and corresponding ADC map (d). (e) Maximum-intensity projection of TOF venogram. These findings may be consistent with prominent cytotoxic edema. The differential diagnosis of hyperacute arterial stroke and venous stroke remains difficult on T2- or T1-weighed SE and DW images.
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Figure 5e. Acute venous infarction (superior sagittal sinus thrombosis) with high signal intensity on DW images and low ADC values. (a) Transverse T2-weighted fast SE image (5500/128 [repetition time/echo time]; 6-mm section thickness; three signals averaged; echo train length, 23; and 230 x 512 matrix). (b) Transverse T1-weighted SE image (550/14), 6-mm section thickness, three signals averaged, one echo, and 192 x 256). (c, d) Transverse DW image (x = sensitizing direction) (c) multishot echo-planar image (800/123, one signal acquired, 6-mm section thickness) and corresponding ADC map (d). (e) Maximum-intensity projection of TOF venogram. These findings may be consistent with prominent cytotoxic edema. The differential diagnosis of hyperacute arterial stroke and venous stroke remains difficult on T2- or T1-weighed SE and DW images.
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Figure 6a. Acute venous infarction with low signal on DW images and increased ADC values (left lateral sinus thrombosis). (a, b) Transverse T2-weighted (a) and T1-weighted (b) SE images. (c, d) Transverse DW (trace) multishot echo-planar image (c) and corresponding ADC map (d). (e) Maximum-intensity projection of phase-contrast venography (20 cm/sec). These findings may be consistent with prominent vasogenic edema.
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Figure 6b. Acute venous infarction with low signal on DW images and increased ADC values (left lateral sinus thrombosis). (a, b) Transverse T2-weighted (a) and T1-weighted (b) SE images. (c, d) Transverse DW (trace) multishot echo-planar image (c) and corresponding ADC map (d). (e) Maximum-intensity projection of phase-contrast venography (20 cm/sec). These findings may be consistent with prominent vasogenic edema.
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Figure 6c. Acute venous infarction with low signal on DW images and increased ADC values (left lateral sinus thrombosis). (a, b) Transverse T2-weighted (a) and T1-weighted (b) SE images. (c, d) Transverse DW (trace) multishot echo-planar image (c) and corresponding ADC map (d). (e) Maximum-intensity projection of phase-contrast venography (20 cm/sec). These findings may be consistent with prominent vasogenic edema.
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Figure 6d. Acute venous infarction with low signal on DW images and increased ADC values (left lateral sinus thrombosis). (a, b) Transverse T2-weighted (a) and T1-weighted (b) SE images. (c, d) Transverse DW (trace) multishot echo-planar image (c) and corresponding ADC map (d). (e) Maximum-intensity projection of phase-contrast venography (20 cm/sec). These findings may be consistent with prominent vasogenic edema.
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Differential Diagnosis with Arterial Stroke
The differential diagnosis of arterial and venous stroke may be impossible with acute-stroke MR protocols (ie, including T2-weighted SE, FLAIR, DW and perfusion-weighted images, and MR arteriography).
For more information, see the section on Acute Infarction.
Background and Discussion
Imaging
The diffusion findings in human cerebral venous infarction remain controversial. Initial reports suggested increased to slightly decreased ADC values with hypo- to isointensity on DW images (15,16). These findings were explained by the presence of prominent vasogenic edema associated with mild cytotoxic edema.
In 1998, Corvol et al (15) reported a case of an extensive thrombosis of the superior sagittal sinus and the left lateral sinus. There was a large frontoparietal hyperintensity on FLAIR images and only a discrete hyperintensity on DW images, with a slight decrease in ADC values (0.53 x 10-3 mm2/sec compared with 0.61 x 10-3 mm2/sec in the contralateral hemisphere). These findings were explained by prominent vasogenic edema associated with mild cytotoxic edema.
In 1999, Keller et al (16) reported the findings in a case of a deep cerebral venous thrombosis with extensive hyperintensities in the basal ganglia on T2-weighted images and hypointensities on DW images, with increased ADC values (1.1-1.6 x 10-3 mm2/sec). These findings were explained by the presence of vasogenic edema. The patient was treated with intravenous heparin, with total clinical recovery and no parenchymal defects at follow-up MR examinations.
More recently, a larger series of cerebral venous infarctions with high signal intensity on DW images and low ADC values were reported (17–19). The findings were attributed to cytotoxic edema.
Manzione et al (17) reported a case of a superior sagittal sinus thrombosis and a right transverse sinus thrombosis with a frontal hyperintensity on T2-weighted images and two more extensive hyperintensities on DW images, associated with an area of severe (0.2 x 10-3 mm2/sec) and an area of moderate (0.3 x 10-3 mm2/sec) reduction in ADC values. The lesion with a severe reduction in ADC values was associated with a small residual lesion at follow-up MR examination, while the area with a moderate reduction in ADC values reversed completely.
Forbes et al (18) studied 12 patients with acute cerebral venous thrombosis. Ten regions of cerebral venous infarction were detected in seven patients, all showing T2 hyperintensity. Two of these regions were predominantly hemorrhagic and did not display diffusion hyperintensity. The remaining eight regions displayed diffusion hyperintensity associated with a decreased ADC.
In a case of a superior sagittal sinus thrombosis reported by Peeters et al (19), the faint hyperintensity on T2-weighted SE and FLAIR images was associated with pronounced hyperintensity on DW images and an important decrease in ADC values in the range of 0.34–0.46 x 10-3 mm2/sec, compared with 0.68 x 10-3 mm2/sec in the contralateral hemisphere.
Presumed Causes of Low and High Signal Intensity on DW Images
The pathophysiologic mechanisms that lead to cerebral venous infarction remain controversial. Traditional models hold that retrograde venous pressure causes a breakdown of the blood-brain barrier, with leakage of fluid (vasogenic edema) and hemorrhage into the extracellular space (20).
Alternatively, a pathway from venous obstruction to infarction has been proposed wherein retrograde venous pressure decreases cerebral blood flow, causing tissue damage in a manner similar to that of arterial infarction (21,22). Furthermore, early decreases in ADC values have been shown in animal models of cerebral venous infarction, implying the presence of cytotoxic edema (22).
In our opinion, a coherent model of the pathogenesis of cerebral venous infarction should combine these two explanations. The initial event in venous infarction is the rise is venous pressure associated with disruption of the capillary tight junctions; this produces an increase in extracellular water (vasogenic edema). These lesions are completely reversible, provided there is successful venous thrombolysis, as reported (15,16). An increase in intracellular water follows (cytotoxic edema), resulting in restriction of water diffusion and hyperintensity on DW images (17–19). The mechanism may be energy failure with loss of sodium-potassium pump activity, as in arterial stroke. The reduction in cerebral blood flow may be an important factor in this process. However, in contrast to arterial stroke, the "bright" lesions on DW images in venous infarction might be more susceptible to complete recovery if successfully treated, as we reported (19). We know from studies with xenon CT in acute human stroke that cerebral blood flow of 6 mL/100g/min will produce irreversible infarction, while the ischemic penumbra with flow values of 7-20 mL/100g/min may be salvaged after restoration of normal flow (23). In venous infarction, hypoperfusion develops progressively. We postulate that it probably seldom falls under the threshold of approximately 6 mL/100g/min, since perfusion of the affected brain tissue might still be possible at lower flow rates if the blood drains through collateral pathways (22). The swollen cells might be functionally but not irreversibly damaged and therefore have a potential for recovery (24).
Conclusions
The differential diagnosis of arterial and venous stroke may be impossible with acute-stroke MR protocols. The diagnosis of venous sinus thrombosis during the first 7 days after the event is not always straightforward with conventional T1- and T2-weighted sequences. Important perfusion abnormalities have also been reported in venous stroke, and normal findings at MR arteriography do not exclude arterial stroke (eg, small branches or early spontaneous recanalization).
The diffusion findings in human cerebral venous infarction remain controversial. Initial reports suggested increased to slightly decreased ADC values with hypo- to isointensity on DW images (15,16). These findings were explained by the presence of prominent vasogenic edema associated with mild cytotoxic edema. More recently, a larger series of cerebral venous infarctions with high signal intensity on DW images and low ADC values have been reported (17–19), and the findings were attributed to cytotoxic edema. The pathophysiologic mechanisms that lead to cerebral venous infarction also remain controversial.
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Tumors: Glioma
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Typical Presentation on DW Images and ADC Maps
The signal intensity of gliomas on DW images is variable (hyper-, iso-, or hypointense) (25,26). Occasionally the gliomas are hyperintense on DW images and show reduced ADC values (suggests reduced volume of extracellular space) or not reduced ADC values (suggests T2 "shine-through" effect) (Fig 7).
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Figure 7a. Glioblastoma multiforme. (a) Transverse T2-weighted fast SE image (5000/128; two signals averaged; 6-mm section thickness; echo train length, 23; matrix, 230 x 512). (b) Transverse T1-weighted nonenhanced SE image (520/14; two signals averaged; 6-mm section thickness; matrix, 179 x 256). (c) Transverse T1-weighted contrast-enhanced SE image (520/14; two signals averaged; 6-mm section thickness; matrix, 179 x 256). (d-f) (d) Transverse multishot echo-planar image (800/123, one signal acquired, 6-mm section thickness), (e) corresponding DW echo-planar image (sensitizing direction = x), and (f) corresponding ADC map. The high signal intensity of cerebrospinal fluid on the multishot echo-planar image (d) is suppressed on the DW echo-planar image (e). The nonnecrotic components of glioblastoma are slightly hyperintense on the DW echo-planar image (T2 shine-through effect). On DW images (e), the peritumoral vasogenic edema is isointense to the white matter because the effect of increased diffusion (dark) is compensated for by the increased T2 values of edema (bright). The peritumoral edema, cerebrospinal fluid, and necrotic component of the tumor are hyperintense (high diffusion) on the ADC map.
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Figure 7b. Glioblastoma multiforme. (a) Transverse T2-weighted fast SE image (5000/128; two signals averaged; 6-mm section thickness; echo train length, 23; matrix, 230 x 512). (b) Transverse T1-weighted nonenhanced SE image (520/14; two signals averaged; 6-mm section thickness; matrix, 179 x 256). (c) Transverse T1-weighted contrast-enhanced SE image (520/14; two signals averaged; 6-mm section thickness; matrix, 179 x 256). (d-f) (d) Transverse multishot echo-planar image (800/123, one signal acquired, 6-mm section thickness), (e) corresponding DW echo-planar image (sensitizing direction = x), and (f) corresponding ADC map. The high signal intensity of cerebrospinal fluid on the multishot echo-planar image (d) is suppressed on the DW echo-planar image (e). The nonnecrotic components of glioblastoma are slightly hyperintense on the DW echo-planar image (T2 shine-through effect). On DW images (e), the peritumoral vasogenic edema is isointense to the white matter because the effect of increased diffusion (dark) is compensated for by the increased T2 values of edema (bright). The peritumoral edema, cerebrospinal fluid, and necrotic component of the tumor are hyperintense (high diffusion) on the ADC map.
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Figure 7c. Glioblastoma multiforme. (a) Transverse T2-weighted fast SE image (5000/128; two signals averaged; 6-mm section thickness; echo train length, 23; matrix, 230 x 512). (b) Transverse T1-weighted nonenhanced SE image (520/14; two signals averaged; 6-mm section thickness; matrix, 179 x 256). (c) Transverse T1-weighted contrast-enhanced SE image (520/14; two signals averaged; 6-mm section thickness; matrix, 179 x 256). (d-f) (d) Transverse multishot echo-planar image (800/123, one signal acquired, 6-mm section thickness), (e) corresponding DW echo-planar image (sensitizing direction = x), and (f) corresponding ADC map. The high signal intensity of cerebrospinal fluid on the multishot echo-planar image (d) is suppressed on the DW echo-planar image (e). The nonnecrotic components of glioblastoma are slightly hyperintense on the DW echo-planar image (T2 shine-through effect). On DW images (e), the peritumoral vasogenic edema is isointense to the white matter because the effect of increased diffusion (dark) is compensated for by the increased T2 values of edema (bright). The peritumoral edema, cerebrospinal fluid, and necrotic component of the tumor are hyperintense (high diffusion) on the ADC map.
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Figure 7d. Glioblastoma multiforme. (a) Transverse T2-weighted fast SE image (5000/128; two signals averaged; 6-mm section thickness; echo train length, 23; matrix, 230 x 512). (b) Transverse T1-weighted nonenhanced SE image (520/14; two signals averaged; 6-mm section thickness; matrix, 179 x 256). (c) Transverse T1-weighted contrast-enhanced SE image (520/14; two signals averaged; 6-mm section thickness; matrix, 179 x 256). (d-f) (d) Transverse multishot echo-planar image (800/123, one signal acquired, 6-mm section thickness), (e) corresponding DW echo-planar image (sensitizing direction = x), and (f) corresponding ADC map. The high signal intensity of cerebrospinal fluid on the multishot echo-planar image (d) is suppressed on the DW echo-planar image (e). The nonnecrotic components of glioblastoma are slightly hyperintense on the DW echo-planar image (T2 shine-through effect). On DW images (e), the peritumoral vasogenic edema is isointense to the white matter because the effect of increased diffusion (dark) is compensated for by the increased T2 values of edema (bright). The peritumoral edema, cerebrospinal fluid, and necrotic component of the tumor are hyperintense (high diffusion) on the ADC map.
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Figure 7e. Glioblastoma multiforme. (a) Transverse T2-weighted fast SE image (5000/128; two signals averaged; 6-mm section thickness; echo train length, 23; matrix, 230 x 512). (b) Transverse T1-weighted nonenhanced SE image (520/14; two signals averaged; 6-mm section thickness; matrix, 179 x 256). (c) Transverse T1-weighted contrast-enhanced SE image (520/14; two signals averaged; 6-mm section thickness; matrix, 179 x 256). (d-f) (d) Transverse multishot echo-planar image (800/123, one signal acquired, 6-mm section thickness), (e) corresponding DW echo-planar image (sensitizing direction = x), and (f) corresponding ADC map. The high signal intensity of cerebrospinal fluid on the multishot echo-planar image (d) is suppressed on the DW echo-planar image (e). The nonnecrotic components of glioblastoma are slightly hyperintense on the DW echo-planar image (T2 shine-through effect). On DW images (e), the peritumoral vasogenic edema is isointense to the white matter because the effect of increased diffusion (dark) is compensated for by the increased T2 values of edema (bright). The peritumoral edema, cerebrospinal fluid, and necrotic component of the tumor are hyperintense (high diffusion) on the ADC map.
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Figure 7f. Glioblastoma multiforme. (a) Transverse T2-weighted fast SE image (5000/128; two signals averaged; 6-mm section thickness; echo train length, 23; matrix, 230 x 512). (b) Transverse T1-weighted nonenhanced SE image (520/14; two signals averaged; 6-mm section thickness; matrix, 179 x 256). (c) Transverse T1-weighted contrast-enhanced SE image (520/14; two signals averaged; 6-mm section thickness; matrix, 179 x 256). (d-f) (d) Transverse multishot echo-planar image (800/123, one signal acquired, 6-mm section thickness), (e) corresponding DW echo-planar image (sensitizing direction = x), and (f) corresponding ADC map. The high signal intensity of cerebrospinal fluid on the multishot echo-planar image (d) is suppressed on the DW echo-planar image (e). The nonnecrotic components of glioblastoma are slightly hyperintense on the DW echo-planar image (T2 shine-through effect). On DW images (e), the peritumoral vasogenic edema is isointense to the white matter because the effect of increased diffusion (dark) is compensated for by the increased T2 values of edema (bright). The peritumoral edema, cerebrospinal fluid, and necrotic component of the tumor are hyperintense (high diffusion) on the ADC map.
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Differential Diagnosis of Ring-enhancing Cerebral Masses
The differential diagnosis of intracerebral necrotic tumors and cerebral abscesses is frequently impossible on conventional MR images. DW MR imaging is a valuable diagnostic test in cases of cerebral "ring-enhancing" masses.
For more information, see the section on Inflammation: Abscess.
Background and Discussion
Signal Intensity of the Solid Portion of Gliomas on DW Images and ADC Maps
The signal intensity of gliomas on DW images is variable (hyper-, iso-, or hypointense), and a subtle hyperintensity is a common nonspecific finding (1,11) (Table 2). The reported ADC values are in the range of 0.82 ± 0.13 to 1.14 ± 0.18 (x 10-3 mm2/sec) (1–11). Tumor cellularity is probably a major determinant of ADC values of brain tumors, although probably not the only one (1,3,11).
Can the ADC Values Differentiate between Different Grades of Gliomas?
ADC values cannot be used in individual cases to differentiate glioma types reliably (the ADCs of patients with grade II astrocytoma and glioblastoma overlap) (25,26,28,29). However, in the study of Kono et al (25), the combination of routine image interpretation and ADC values had a higher predictive value. In the study of Gauvain et al (28), there was a clear distinction between the low-grade gliomas and the embryonal tumors (the ADC values for low-grade gliomas were 1.33 x 10-3 mm2/sec ± 0.21 (range, 1.132–1.60), for nonembryonal high-grade tumors the ADC values were 1.22 x 10-3 mm2/sec ± 0.09 (range, 1.128–1.303) and for the group of embryonal tumors (primitive neuroectodermal tumor, medulloblastoma, malignant teratoid-rhabdoid tumor) the ADC values were 0.72 x 10-3 mm2/sec ± 0.20 (range, 0.538–0.974).
Can the DW Images and/or ADC Maps Differentiate between Glioma and Peritumoral Edema?
The majority of recent studies report that DW images and/or ADC maps cannot distinguish neoplastic cell infiltration from peritumoral edema in patients with malignant glioma (25,26,28,29). In 1995, Tien et al (30) could distinguish areas of peritumoral neoplastic cell infiltration from predominantly peritumoral edema when abnormalities were located in the white matter aligned in the direction of the DW gradient. However, Recent findings do not support the hypothesis that peritumoral neoplastic cell infiltration can be depicted by means of ADCs or ADC maps (25,26,28,29).
Conclusions
The signal intensity of gliomas on DW images is variable (hyper-, iso-, or hypointense) (25,26). Occasionally, gliomas are hyperintense on DW images and show reduced ADC values (suggests reduced volume of extracellular space) or not reduced ADC values (suggests T2 shine-through effect). Tumor cellularity is probably a major determinant of ADC values of brain tumors. ADC values cannot be used in individual cases to differentiate glioma types reliably. DW images and/or ADC maps cannot distinguish neoplastic cell infiltration from peritumoral edema in patients with malignant glioma (25,26,28,29).
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Tumors: Metastases
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Typical Presentation on DW Images and ADC Maps
The reported cases of metastases were isointense to slightly hyperintense on DW images, and the calculated ADC values were in the range 0.82–1.24 x 10-3 mm2/sec (26).
In our experience, the signal intensity of nonnecrotic components of metastases on DW images is variable (generally iso- or hypointense; occasionally hyperintense). The necrotic components of metastases show a marked signal suppression on DW MR images and increased ADC values (31). The increased signal intensity on DW images and a low ADC value are unusual but possible (32) (Figs 8, 9).
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Figure 8a. Multiple metastases. (a) Axial T2-weighted fast SE, (b, c) T1-weighted (b) nonenhanced and (c) contrast-enhanced SE, and (d) DW (trace) images and (e) corresponding ADC map.
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Figure 8b. Multiple metastases. (a) Axial T2-weighted fast SE, (b, c) T1-weighted (b) nonenhanced and (c) contrast-enhanced SE, and (d) DW (trace) images and (e) corresponding ADC map.
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Abstract
Basic Physics of Diffusion...
