Imaging Tutorial - Differential Diagnosis of Bright Lesions On Diffusion-Weighted MR Images - RadioGraphics

!
# $
" Menu
Home > RadioGraphics > Vol. 23, No. 1
NEXT %
Online Only & Free Access
Imaging Tutorial: Di!erential Diagnosis of Bright

Lesions on Di!usion-weighted MR Images
Tadeusz W. Stadnik, Philippe Demaerel, Robert R Luypaert, Christo Chaskis,
Katrijn L. Van Rompaey, Alex Michotte, Michel J. Osteaux
' Author A"liations
1From 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 scienti!c exhibit at the 2001 RSNA scienti!c 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).
Published Online: Jan 1 2003https://doi.org/10.1148/rg.e7
Abstract
High sensitivity (94%) and speci!city (100%) have been reported in the diagnosis of acute cerebral
infarction with di"usion-weighted magnetic resonance (MR) imaging. However, high signal
intensity on di"usion-weighted MR images and low apparent di"usion coe#cient values (similar to
the !ndings in acute cerebral infarction) were reported in such diverse conditions as hemorrhage,
abscess, lymphoma, and even Creutzfeldt-Jakob disease. The di"erential diagnosis of these
:
conditions (eg, acute ischemic infarction and acute cerebral hemorrhage)
( Back is critical for the
determination of appropriate treatment. The authors present a systematic review of bright lesions
on di"usion-weighted MR images and their di"erential diagnosis, with emphasis on the practical
and clinical approaches of di"erential diagnosis.
© RSNA, 2002
Basic Physics of Di!usion-weighted (DW) Magnetic

Resonance (MR) Imaging
This topic was covered in an article titled Di"usion imaging: from basic physics to practical imaging,
published in RSNA EJ/RadioGraphics in 1999.
Acute Infarction
Typical Presentation on DW Images and Apparent Di!usion

Coe"cient (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 $ow 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).
Di!erential Diagnosis with Venous Stroke

Di"erential diagnosis of arterial and venous stroke may be impossible with use of acute-stroke MR
imaging protocols (ie, T2-weighted SE, $uid-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 !ndings at MR arteriography do not exclude arterial stroke (eg, small
branches or early spontaneous recanalization).
Hints for di!erential 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
Di!erential Diagnosis with Cerebritis

,,,,,
:
The di"erential 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.
•. See the section on In!ammation: 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 di"usion 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 “$ip-$op” from dark to bright 7-10 days later (,4–,8). This property
may be used to di"erentiate 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 di"usion is
relatively restricted (,1).
What are the Sensitivity and Speci"city of DW images and ADC Maps in Acute Stroke?
The majority of studies report high sensitivity and speci!city for DW images and ADC maps in the
diagnosis of acute stroke (94%sensitivity and 100%speci!city in the study by Lövblad et al [,11]
within the !rst 6 hours after stroke; 100%sensitivity and 100%speci!city 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 !nal diagnosis of acute
stroke, and DW images were negative in eight patients, all of whom had a !nal 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 !nding (,13,,14). The potential mechanism
that may explain the lack of di"usion changes in the acute phase in these patients is that cerebral
blood $ow was at an intermediate level below the threshold for neuronal dysfunction (symptom
onset) but above that of reduced di"usion (,1).
:
Conclusions
The signal intensity of acute stroke on DW images increases during the 1st week after symptom
onset and decreases thereafter, but signal remains hyperintense for a long period. The ADC values
decline rapidly after the onset of ischemia and subsequently increase with the “$ip-$op” from dark
to bright 7-10 days later. This property may be used to di"erentiate the lesions older than 10 days
from more acute ones. Most studies report high sensitivity and speci!city for DW images and ADC
maps in the diagnosis of acute stroke. There have been only occasional reports of patients
progressing to complete stroke after an initial negative DW imaging !nding. The di"erential
diagnosis of arterial and venous stroke may be impossible with acute-stroke MR protocols (ie,
including T2-weighted SE, FLAIR, DW and perfusion-weighted imaging, and MR arteriography). The
clinical presentation and early hemorrhage, especially when near the venous sinuses, should
prompt performance of MR or CT venography.
Venous Infarction
Typical Presentation on DW Images and ADC Maps
Di"usion !ndings in human venous infarction have so far been limited to con$icting case reports.
The initial reports suggested increased to slightly decreased ADC values with hypo- to isointensity
on DW images (,15,,16). These !ndings 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 !ndings
were attributed to cytotoxic edema (,,,,,,Figs 5, ,,,,,6).
Di!erential Diagnosis with Arterial Stroke

The di"erential 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.

Imaging
The di"usion !ndings 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 !ndings 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
-3 2
:
a discrete hyperintensity on DW images, with a slight decrease in ADC values (0.53 × 10-3 mm2/sec
compared with 0.61 × 10-3 mm2/sec in the contralateral hemisphere). These !ndings were
explained by prominent vasogenic edema associated with mild cytotoxic edema.
In 1999, Keller et al (,16) reported the !ndings 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 × 10-3 mm2/sec). These !ndings 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 !ndings 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 × 10-3 mm2/sec) and an area
of moderate (0.3 × 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 di"usion hyperintensity. The
remaining eight regions displayed di"usion 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 ×
10-3 mm2/sec, compared with 0.68 × 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 $uid (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 $ow, 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 di"usion 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 $ow 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 $ow of 6
mL/100g/min will produce irreversible infarction, while the ischemic penumbra with $ow values of
7-20 mL/100g/min may be salvaged after restoration of normal $ow (,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 a"ected brain tissue might still
be possible at lower $ow 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 di"erential diagnosis of arterial and venous stroke may be impossible with acute-stroke MR
protocols. The diagnosis of venous sinus thrombosis during the !rst 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 !ndings at MR arteriography
do not exclude arterial stroke (eg, small branches or early spontaneous recanalization).
The di"usion !ndings 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 !ndings 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 !ndings
were attributed to cytotoxic edema. The pathophysiologic mechanisms that lead to cerebral
venous infarction also remain controversial.
Tumors: Glioma

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”
e"ect) (,,,,,,,Fig 7).
Di!erential Diagnosis of Ring-enhancing Cerebral Masses

The di"erential 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 In$ammation: Abscess.

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 nonspeci!c !nding (,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 Di!erentiate between Di!erent Grades of Gliomas?
ADC values cannot be used in individual cases to di"erentiate 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 × 10-3
mm2/sec ± 0.21 (range, 1.132–1.60), for nonembryonal high-grade tumors the ADC values were
1.22 × 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 × 10-3 mm2/sec ± 0.20 (range, 0.538–0.974).
Can the DW Images and/or ADC Maps Di!erentiate between Glioma and Peritumoral Edema?
The majority of recent studies report that DW images and/or ADC maps cannot distinguish
neoplastic cell in!ltration 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
in!ltration from predominantly peritumoral edema when abnormalities were located in the white
matter aligned in the direction of the DW gradient. However, Recent !ndings do not support the
hypothesis that peritumoral neoplastic cell in!ltration 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
e"ect). Tumor cellularity is probably a major determinant of ADC values of brain tumors. ADC
values cannot be used in individual cases to di"erentiate glioma types reliably. DW images and/or
ADC maps cannot distinguish neoplastic cell in!ltration from peritumoral edema in patients with
malignant glioma (,25,,26,,28,,29).
:
Tumors: Metastases
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 × 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).
Figures 8 and 9 show a typical presentation of cerebral metastases with variable signal intensity of
nonnecrotic components on DW images (,,,,,,,Fig 9d) and ADC values similar to the white matter
(,,,,,,,Fig 9f). The necrotic components of metastases show a marked signal suppression on DW MR
images and increased ADC values (,,,,,,Fig 8d,,,,,,,8e).
Di!erential Diagnosis of Ring-enhancing Cerebral Masses

The di"erential diagnosis of intracerebral necrotic metastases (,,,,,Fig 10) and cerebral abscesses is
frequently impossible on conventional MR images. DW imaging is a valuable diagnostic test in
cases of cerebral ring-enhancing masses.
On the T2-weighted fast SE (,,,,,Fig 10a) and the contrast-enhanced T1-weighted SE (,,,,,Fig 10b)
images the di"erential diagnosis of metastasis and abscess is impossible. The central
hypointensity on the DW image (,,,,,Fig 10c) and the hyperintensity on the ADC map (,,,,,Fig 10d)
support the diagnosis of necrotic metastasis
For more information, see the section on In$ammation: Abscess

DW imaging of cerebral metastases has received only limited attention. In the reported cases, the
solid components of cerebral metastases were isointense to slightly hyperintense on DW images
and the calculated ADC values were in the range 0.82–1.24 × 10-3 mm2/sec (,26).

variable (generally iso- or hypointense, occasionally hyperintense).
The necrotic components of cerebral metastases show a marked signal suppression on DW images
and increased ADC values (mean value of 2.62 × 10-3 mm2/sec [n = 7] in the report of Krabbe et al
[,31]). The increased signal intensity on DW images and a low ADC value are unusual but possible.
Tung et al reported two metastases, both squamous cell carcinomas, with markedly increased
signal intensity on DW images and a low ADC value (,32). However, this presentation was unusual.
:
In the same report, only !ve of 30 rim-enhanced masses had high signal intensity on DW images
and low ADC values; two of these !ve cases were brain abscesses, two were the metastases from
lung squamous cell carcinoma, and one was radiation necrosis (,32). In a report by Hartmann et al
(,33), only one metastasis of eight had high signal intensity on DW images and low ADC values
(,,,,,,Fig 11).
Tumor cellularity is probably a major determinant of signal intensity of solid components of

cerebral metastases on DW images and on ADC values. The signal intensity of necrotic
components of cerebral metastases may be related to increased free water (usual presentation:
low signal intensity on DW images, high ADC values) and/or presence of extracellular
methemoglobin and/or increased viscosity (unusual presentation: high signal intensity on DW
images, low ADC values).
Conclusions
variable (generally iso- or hypointense, occasionally hyperintense). The necrotic components of
metastases show a marked signal suppression on DW images and increased ADC values (may be
related to increased free water). Increased signal intensity on DW images and a low ADC value are
unusual but possible (may be related to the presence of extracellular methemoglobin and/or
increased viscosity).
Tumors: Meningioma
Typical presentation on DW images and ADC maps
The signal intensity of meningiomas on DW images is variable (hyper-, iso-, or hypointense)
(,26,,34). Most benign meningiomas are isointense on DW images and ADC maps (,,,,,,,Figs 12, ,,,,,,13)
(,26,,34). Only 23%of benign meningiomas (three of 13) were slightly hyperintense in the study of
Filippi et al (,34). In the same study, four malignant meningiomas had markedly increased signal
intensity on DW images, decreased signal intensity on ADC maps, and low ADC values (,34).

The signal intensity of meningiomas on DW images is variable (hyper-, iso-, or hypointense) (,Table
3) (,26,,34). Most benign meningiomas are isointense on DW images and ADC maps (,26,,34). Only
23%of benign meningiomas (three of 13) were slightly hyperintense in the study of Filippi et al (,34).
On average, these meningiomas had an elevated ADC value (average, 1.03 × 10-3 mm2/sec ± 0.29;
range, 0.62–1.80 × 10-3 mm2/sec) with the exception of densely calci!ed or psammomatous
meningiomas, which may have a low ADC (0.62 × 10-3 mm2/sec). In the same study, four malignant
meningiomas had markedly increased signal on DW images, hypointense signal on ADC maps, and
low ADC values indicative of marked restriction to water di"usion. All these meningiomas had T2-
and T1-weighted imaging characteristics suggestive of benign disease, including homogeneous
signal intensity similar to that of gray matter, intense homogeneous enhancement (no cystic,
:
necrotic, or hemorrhagic foci), smooth and distinct margins, and no evidence of brain invasion.
Atypical or malignant histopathologic results were not anticipated on the basis of routine MR
imaging. Tumor cellularity is probably a major determinant of ADC values of brain tumors,
although probably not the only one (,26,,34).
Can the DW images and ADC values di"erentiate between malignant and benign meningiomas?
Considering the report of Filippi et al (,34), DW imaging is a valuable diagnostic test in the
di"erential diagnosis of malignant and benign meningiomas. (Four malignant or atypical
meningiomas (World Health Organization [WHO] grades II and III) were extremely hyperintense on
the DW images (“lightbulbs”) and hypointense on the corresponding ADC maps and had markedly
decreased ADC values. Thirteen benign meningiomas (WHO grade I) were hyper-, iso-, or
hypointense on the DW images and on the corresponding ADC maps and had increased ADC
values, with the exception of one case of a densely calci!ed meningioma (iso- to hypointense on
DW images and iso- to hyperintense on the ADC map (ADC = 0.62 × 10-3 mm2/sec. In our
experience, benign meningiomas may also show high signal intensity on DW images and reduced
ADC values.
Conclusions
The signal intensity of meningiomas on DW images is variable (hyper-, iso-, or hypointense)
(,26,,34). Most benign meningiomas are isointense on DW images and ADC maps (,26,,34). Only
23%of benign meningiomas were slightly hyperintense (three of 13) in the study of Filippi et al (,34).
On average, these meningiomas had an elevation in the ADC value. High signal intensity on DW
images and reduced ADC values (average, 0.53 × 10-3 mm2/sec ± 0.12; range, 0.40–0.69 × 10-3
mm2/sec) suggest malignant meningioma (,34). In our experience, however, benign meningiomas
may also show high signal intensity on DW images and reduced ADC values.
Tumors: Lymphoma
Typical Presentation on DW images and ADC Maps
The enhancing components of lymphomas are generally hyperintense on DW images (,,,,,,Fig 14).
Di!erential Diagnosis
The di"erential diagnosis of cerebral lymphoma, metastases, and glial tumors is frequently
impossible on conventional MR images (,,,,,Figs 15, ,,,,,16). A large study is needed to con!rm the
potential utility of DW imaging in cases of cerebral lymphoma.
•. A majority of lymphomas are either isointense or hypointense relative to gray matter on T2-
weighted images (33% and 20%, respectively, in the study of Johnson et al [,35]).
•. Most lymphomas identi"ed on long TR images enhance (homogeneous enhancement in
:
immunocompetent patients; rim enhancement is more common in immunocompromised
patients [,36–,39]).
•. High signal intensity on DW images and low ADC values may favor the diagnosis of lymphoma
versus glioma or metastasis (,26).

In the reported cases of cerebral lymphomas, enhancing components were hyperintense on DW
images and the contrast with white matter was as high as 9.4. An additional case of cerebral
lymphoma showed a mixture of hyperintense and hypointense components, however (,26). This
may be related to necrosis. The reported ADC values were as low as 0.58 and 0.55 × 10-3 mm2/sec
± 0.18 (,26). Tumor cellularity is probably a major determinant of ADC values of cerebral
lymphomas (,26).
Conclusions
The initial reports suggest that the enhancing components of lymphomas are hyperintense on DW
images and show low ADC values. A large study is needed to con!rm the potential utility of DW
imaging in the di"erential diagnosis of cerebral lymphomas, metastases, and glial tumors.
Tumors: Epidermoid Cyst

Epidermoid tumors are isointense to slightly hyperintense relative to cerebrospinal $uid on T1-,
T2-, and proton density-weighted images (,40‐,44); it is di#cult to discern the exact extension of an
epidermoid tumor with only T1-, T2-, or proton density-weighted imaging. On DW images,
epidermoid tumors show high signal intensity and are easily di"erentiated from cerebrospinal
$uid or arachnoid cysts (,,,,,Figs 17, ,,,,,18) (,45). Constructive interference in the steady state (CISS)
and FLAIR sequences also depict epidermoid tumors in the subarachnoid spaces better than
conventional SE images (,46). The reported mean ADC value of epidermoid tumors was 1.197 × 10-3
mm2/sec (47–50. In our experience, the ADC values of epidermoid cyst and gray and white matter
are similar. Therefore, the high signal intensity of epidermoid cysts on DW images suggests the T2
shine-through e"ect.
Di!erential Diagnosis with Arachnoid Cyst
The di"erential diagnosis of epidermoid and arachnoid cyst is straightforward on DW images. The
epidermoid cyst is bright, while the arachnoid cyst is dark. CISS and FLAIR sequences are also
useful.
•. Signal intensity on DW imges, ADC maps, CISS images, and FLAIR images (,Table 4)
•. Epidermoid tumors insinuate along CSF spaces and encase arteries and cranial nerves,
,
:
whereas arachnoid cyst displace adjacent structures (,51).

Epidermoid tumors are benign congenital developmental tumors, usually located in the sellar and
suprasellar regions, the middle fossa, or o" the midline in the posterior fossa. The cysts are thin-
walled and lined with strati!ed squamous epithelium. Cystic contents usually include debris,
keratin, water, and cholesterol. On short repetition time/echo time (TR/TE) MR sequences,
epidermoid tumors typically show mild hypointensity, usually between that of CSF and brain
parenchyma and do not enhance with contrast material. On long TR/TE sequences, these tumors
show hyperintensity, similar to or greater than that of CSF. It is di#cult to discern the exact
extension of an epidermoid tumor with only T1-, T2-, or proton density-weighted imaging. On DW
images, epidermoid tumors have high signal intensity and are easily di"erentiated from CSF or
arachnoid cyst (,45,,50). Ikushima et al reported that CISS and FLAIR sequences also depict
epidermoid tumors in the subarachnoid spaces better than conventional SE images (,46). FLAIR
imaging may give an incorrect demarcation of the lesion, however, because of CSF $ow artifacts.
Echo-planar DW imaging has the best conspicuity of the !ve MR imaging methods (T2-, T1-, proton
density-weighted SE, FLAIR, DW) tested by Chen et al (,50). The reported mean ADC value of
epidermoid tumors was 1.197 × 10-3 mm2/sec (,50). In our experience, the ADC values of
epidermoid cyst and of gray and white matter are similar. Therefore, the high signal intensity of
epidermoid tumors on DW images suggests the T2 shine-through e"ect.
Conclusions
It is di#cult to discern the exact extension of an epidermoid tumor by using only T1-,T2-, or proton
density-weighted imaging. The di"erential diagnosis of arachnoid cyst may also be impossible on
T2-, T1-, and proton density-weighted SE images, whereas it is straightforward on DW images. On
the latter, the epidermoid cyst is bright while the arachnoid cyst is dark. The ADC values of
epidermoid cyst and of gray and white matter are similar. Therefore, the high signal intensity of
epidermoid cysts on DW images is related to the T2 shine-through e"ect.
In#ammation: Abscess
The reported cases of cerebral abscess showed central hyperintensity on DW echo-planar images
(,,,,,Fig 19) and strongly reduced ADC values (range, 0.27–0.64 × 10-3 mm2/sec) (,52–,56)
Di!erential Diagnosis of Abscess and Acute Ischemic Stroke

During the initial cerebritis stage (an ill-de!ned subcortical hyperintense zone on T2-weighted
images associated with poorly delineated enhancing areas within the iso- to mildly hypointense
edematous region on enhanced T1-weighted images) (,57), the di"erential diagnosis of abscess
and acute ischemic stroke may be di#cult.
:
•. Clinical presentation (typically acute onset in ischemic stroke).

•. Parenchymal contrast material uptake (unusual in subacute ischemic stroke).
•. ADC values (reported ADC values of cerebral abscesses are ±50% lower than those of
ischemic stroke after 8 hours).
Di!erential Diagnosis of Abscess and Cystic or Necrotic Tumors

The di"erential diagnosis of intracerebral necrotic tumors and cerebral abscesses is frequently
impossible on conventional MR images. The DW image is a diagnostic clue in cases of a cerebral
ring-enhancing mass. Pyogenic brain abscess has been reported to have markedly increased signal
intensity on DW images and markedly decreased signal intensity on ADC maps, while the opposite
happens in necrotic tumors (,,,,,Fig 20). However, Tung et al recently reported two metastases, both
squamous cell carcinomas, and one case of radiation necrosis with markedly increased signal
intensity on DW images and a low ADC value (,32). They speculate that restricted di"usion in these
cases was due to sterile liquefaction necrosis.
•. Presentation on DW images and ADC values. The cystic or necrotic components of tumors
show marked signal suppression on DW images, similar to that of the CSF, and the reported
ADC values are in the range of 2.2 × 10-3 mm2/sec ± 0.9 (,30) and 1.65–2.62 × 10-3 mm2/sec
(,31).

Imaging
The MR features of brain abscesses vary with lesion stage. During the initial cerebritis stage, an ill-
de!ned subcortical hyperintense zone on T2-weighted images is associated with poorly delineated
enhancing areas within the iso- to mildly hypointense edematous region on contrast-enhanced T1-
weighted images (,57). During the early and late capsule stages, the collagenous abscess capsule is
visible on unenhanced images as a comparatively thin-walled, well-delineated iso- to slightly
hyperintense ring that becomes hypointense with T2-weighted sequences (,57). Nonetheless, a
ring-enhancing mass is a nonspeci!c imaging !nding that can be seen in various nonin$ammatory
benign and neoplastic processes. The di"erential diagnosis includes primary brain tumors (eg,
necrotic glioblastoma), metastases, resolving hematoma, infarction, and even demyelinating
disease (,57). Lövblad et al (,11) reported only two false-positive !ndings in 194 cases of acute
ischemic stroke. One false-positive !nding was a cerebral abscess, and the other was a brain
tumor. ADC values, however, were not calculated in this study (,11), and the T2 shine-through
e"ect remains a possible explanation for these !ndings. The reported ADC values for acute
ischemic stroke vary with time. Lutsep et al (,7) reported ADC values of 0.29–0.33 × 10-3 mm2/sec
for ischemic lesions studied less than 8 hours after symptom onset, 0.61 × 10-3 mm2/sec ± 0.14 at
-3 2
:
8–24 hours, and 0.51 × 10-3 mm2/sec ± 0.18 at 1–8 days. Mean normal ADC values for the entire
group (n = 26) were 0.88 × 10-3 mm2/sec ± 0.12. The reported mean ADC values in the central part
of the abscess are ±50%lower than ADC values of ischemic stroke after 8 hours (0.29 and 0.27 × 10-
3 mm2/sec in the study of Desprechins et al [,52], 0.31 × 10-3 mm2/sec in the report of Ebisu et al
[,53]). Increased signal intensity on DW images was also reported in a case of subdural empyema
(,54). On the other hand, the cystic or necrotic components of tumors show a marked signal
suppression on DW images, similar to that of CSF, and the calculated ADC values are in the range
of 2.2 × 10-3 mm2/sec ± 0.9 (,30,,52,,55). However, recently Tung et al reported two metastases,
both squamous cell carcinomas, and one case of radiation necrosis with markedly increased signal
intensity on DW images and a low ADC value (,32). However, this presentation was unusual. Only
!ve of 30 rim-enhancing masses had high signal intensity on DW images and low ADC values; two
of these !ve cases were brain abscesses, two were metastases from lung squamous cell
carcinoma, and one was radiation necrosis.
Presumed Causes of High Signal Intensity on DW Images
These !ndings support the idea that reduced ADC values in the central part of the abscess are
related to the presence of pus. Ebisu et al (,53) performed in vitro DW imaging of aspirated pus, as
well as ADC measurements. The pus imaged in vitro showed high signal intensity and low ADC
values, similar to the results of the in vivo study. He concluded that the pus structure itself is
responsible for the low ADC values, and that the heavily impeded water mobility of pus may be
related to its high cellularity and viscosity. The presence of large molecules, such as !brinogen,
also may play a key role in restricting the di"usion of protons in pus (,58).
Conclusions
Brain abscesses are potentially fatal lesions, and a correct diagnosis should be established as soon
as possible. Establishing the di"erential diagnosis of intracerebral necrotic tumors and cerebral
abscesses is frequently impossible with conventional MR imaging. DW imaging and ADC maps are
useful in the di"erential diagnosis of ring-enhancing cerebral masses. The presence of central
hyperintensity on DW images and low ADC values strongly suggest the presence of pus and
abscess. The di"erential diagnosis includes acute infarction, which also shows hyperintensity on
DW images and reduced ADC values. Nevertheless, the ring enhancement in acute ischemic stroke
is unusual, and ADC values are higher after 8 hours. The ring-enhancing mass with central
hypointensity on DW images and an increase in ADC values suggest necrotic tumor, most
frequently cerebral glioma or metastasis. For these reasons, DW imaging and calculations of ADC
values should be performed in all cases of ring-enhancing cerebral masses.
In#ammation: Granuloma

The reported case of granuloma was hyperintense on DW images, and the calculated ADC values
were decreased (0.39 × 10-3 mm2/sec) (,26). In our experience, the increased signal intensity on DW
,,,,,,
:
images and a low ADC value are usual in in$ammatory granulomas (,,,,,,Fig 21).
Di!erential Diagnosis of Granulomas and Nodular Cerebral

Metastases
The di"erential diagnosis of intracerebral nodular metastases and cerebral granulomas is
frequently not possible on either conventional MR images or DW images. Nodular metastases
frequently show high signal intensity on DW images and low ADC values (related to high cellularity
and/or hemorrhage) (,,,,,,Figs 22, ,,,,,,23).
Conclusions
Experience with di"usion !ndings in cerebral granulomas is limited (,26). In our experience, the
di"erential diagnosis of intracerebral nodular metastases and cerebral granulomas is frequently
not possible on either conventional MR images or DW images.
In#ammation: Encephalitis

Herpes encephalitis lesions are characterized by marked hyperintensity on DW images and
reduced ADC values (48%–66%of that of normal brain parenchyma) (,59). On follow-up T1- and T2-
weighted MR images, these areas demonstrate encephalomalacic change (,,,,Fig 24) (,59). All eight
patients with Nipah virus infection reported by Lim et al (,60) had multiple small bilateral foci within
the subcortical and deep white matter on T2-weighted images. In !ve patients, DW images showed
increased signal intensity.
Di!erential Diagnosis
Hints for di!erential diagnosis herpes encephalitis versus in"ltrative temporal lobe glial tumors:
•. If con"rmed, the hyperintensity on DW images and reduced ADC values favor the diagnosis of
herpes encephalitis.
•. Biological tests (polymerase chain reaction test).
The di"erential diagnosis between acute ischemic stroke and herpes encephalitis may be
problematic on DW images.
Hints for di!erential diagnosis herpes encephalitis versus ischemic stroke:
•. Clinical presentation (acute onset in ischemic stroke, more progressive in herpes

encephalitis).
•. Biological tests (polymerase chain reaction test).
:
Herpes encephalitis lesions are characterized by marked hyperintensity on DW images and
reduced ADC values (48%–66%of the normal brain parenchyma) (,59). On follow-up T1- and T2-
weighted MR images, these areas demonstrate encephalomalacic change (,59). DW images may aid
in distinguishing herpes lesions from in!ltrative temporal lobe tumors because the ADCs of herpes
lesions are low while the ADCs of various tumors are elevated or in the normal range (,26,,30,,59).
All eight patients with Nipah virus infection reported by Lim et al (,60) had multiple small bilateral
foci within the subcortical and deep white matter on T2-weighted images. In !ve patients, DW
images showed increased signal intensity. The restricted di"usion is explained by cytotoxic edema
in tissue undergoing necrosis (,59).
Conclusions
Initial reports suggest that herpes encephalitis lesions are characterized by marked hyperintensity
on DW images and reduced ADC values (48%–66%of those of normal brain parenchyma) (,59).
Hemorrhage

High signal intensity on DW images is reported in hyperacute (intracellular oxyhemoglobin) and
late subacute (extracellular methemoglobin) stages of hemorrhage (,,,,,Figs 25, ,,,,,26; ,Table 5)
(,61,,62). The ADC values are reported to be decreased (,61) or normal (,62) in hyperacute stages
and increased in the late subacute stage (,61).
Di!erential Diagnosis with Hyperacute Ischemic Stroke

The di"erential diagnosis of hyperacute ischemic stroke and hemorrhage may be impossible on
DW images and ADC maps alone. Therefore, the conjoint use of DW images and ADC maps with
T2-weighted SE or T2*-weighted gradient-echo and/or T2-weighted echo-planar images, especially
during the therapeutic window for thrombolysis (up to 3 hours after onset), is mandatory in
di"erentiating hyperacute stroke from hyperacute hemorrhage.
•. In hyperacute ischemic stroke the T2-weighted SE and T2*-weighted gradient-echo "ndings

are normal.
•. In hyperacute hemorrhage, heterogeneous hyperintensity with a hypointense rim is seen on
T2-weighted SE and T2*-weighted gradient-echo images.

The MR appearance of evolving intracranial hemorrhage and its underlying biophysical basis are
:
somewhat complex on conventional MR images and even more on DW images. High signal
intensity on DW images is reported in hyperacute (intracellular oxyhemoglobin) and late subacute
(extracellular methemoglobin) stages of hemorrhage (,61,,62). The ADC values are reported to be
decreased (,61) or normal (,62) in hyperacute stages and increased in the late subacute stage (,61).
Hyperacute Stage (intracellular oxyhemoglobin)
Atlas et al reported two cases of hyperacute hematomas (,61). The signal intensity on DW images
was not reported. The ADC values were 0.1 and 0.54 × 10-3 mm2/sec. In this study the ADC
measurements of all hematomas with intact red cell membranes (including hyperacute, acute, and
even early subacute) were signi!cantly reduced compared with normal brain tissue (,61).
Postulated biophysical explanations for the observed restriction of di"usion in early stages of
intracranial hemorrhage have included:
1. A shrinkage of the extracellular space with clot retraction (,63).

2. A change in the osmotic environment once blood becomes extravascular, which alters the
shape of red blood cells (,64).
3. A phenomenon related to the formation of the "brin network associated with clot (,65).
4. A conformational change of the hemoglobin macromolecule within the red blood cell (,66).
Maldjian et al reported four cases of hyperacute hematoma with high signal intensity on DW
images (,62). The ADC values were in the range 0.47–0.81 (mean, 0.63) × 10-3 mm2/sec. There was
no signi!cant di"erence in the mean trace ADC values (calculated by using the method of expected
values) between hematomas that were bright on T2-weighted images (mean, 0.631 × 10-3
mm2/sec, SD = 0.14), hematomas that were dark on T2-weighted images (mean, 0.739 × 10-3
mm2/sec, SD = 0.22), and contralateral white matter regions (mean, 0.830, SD = 0.20, P = .36).
These results are in complete disagreement with the previous study (,61). The possible explanation
is the “T2 blackout e"ect,” which is the corollary of the T2 shine-through e"ect. Hematomas that
are dark on T2-weighted images have very low signal intensity, often at the level of the background
noise, and obtaining accurate di"usion trace measurements may be $awed by background
masking (a commonly used data processing strategy to reduce computational load by limiting the
voxels in an analysis). Thus, arti!cially low estimates for di"usion trace values can be obtained in
any areas that have signal intensities in the range of the background (hematomas, hemorrhagic
strokes) and in which background masking was used (,62). In our experience (four cases), the
hyperacute hemorrhage was hyperintense on DW images, with heterogeneous hypointense
components and reduced-to-normal ADC values (,Table 6).
As shown in ,Table 6, the ADC values drop with time after onset. This may be related to the relative
concentration of oxy- and deoxyhemoglobin (increasing T2 blackout e"ect of deoxyhemoglobin for
older hematomas).
Late Subacute Stage (extracellular methemoglobin)
Atlas et al reported three cases of late subacute hematoma (,61). The signal intensity on DW
images was not reported. The ADC values were in the range 0.99–1.05 (mean, 1.02) × 10-3
2
:
mm2/sec). They hypothesized that hematomas in which red blood cell membranes have lysed
show considerably more di"usion (higher ADC values). In our experience (six cases), late subacute
hematomas were strongly hyperintense on DW images, with ADC values in the range of 0.12–0.63
(mean, 0.48 SD = 0.33) × 10-3 mm2/sec. Because the ADC values of intracellular oxyhemoglobin and
extracellular methemoglobin are not decreased, the hyperintensity on DW images must be related
to T2 and T1 shine-through e"ects.
Conclusions
The recognition of early intracranial hemorrhage, speci!cally on MR images, has become
important because the primary assessment of patients with early stroke is moving toward MR
imaging and away from CT scanning. As DW imaging becomes integrated into the initial emergent
evaluation of patients with acute stroke (,10,,12,,67), it becomes paramount to understand the
manifestations of intracranial hemorrhage on DW MR imaging speci!cally. The di"erential
diagnosis of hyperacute ischemic stroke and hemorrhage may be impossible on DW images and
ADC maps alone. Therefore, the conjoint use of DW imaging and ADC maps with T2-weighted SE,
T2*-weighted gradient-echo, and/or T2-weighted echo-planar imaging, especially during the
therapeutic window for thrombolysis (up to 3 hours after onset), is mandatory in di"erentiation of
hyperacute stroke from hyperacute hemorrhage. High signal intensity on DW images has been
reported in hyperacute (intracellular oxyhemoglobin) and late subacute (extracellular
methemoglobin) stages of hemorrhage (,61,,62). The ADC values are reported to be decreased (,61)
or normal (,62) in hyperacute stages and increased in the late subacute stage (,61).
Multiple Sclerosis

In our experience, the signal intensity of multiple sclerosis (MS) on DW images is variable (hyper-,
iso-, or hypointense) (,,,,,,,,Fig 27). Gass et al (,68) reported that enhancing lesions were hyperintense
relative to white matter on DW images, while chronic lesions were isointense. Most studies focus
on ADC values in MS. These studies show an increase in ADC values in MS lesions and perhaps also
in the ADC values of normal-appearing white matter of MS patients (,69‐,74). Therefore, we can
hypothesize that the increased intensity in MS lesions on DW images results from the T2 shine-
through e"ect.

In our experience, the signal intensity of MS on DW images is variable (hyper-, iso-, or
hypointense). Gass et al (,68) reported that enhancing lesions were hyperintense relative to white
matter on DW images while chronic lesions were isointense. The same authors reported decreased
ADC values at the borders of some acute plaques, which they attributed to hypercellularity or
cytotoxic edema. This report contains some of the !rst evidence that there may actually be
decreases in ADC associated with an MS lesion (,68). In the study of Roychowdhury et al (,74), four
of 28 homogeneously enhancing lesions had trace ADC values that were 2 SDs below the mean for
:
normal-appearing white matter, while none of the ring-enhancing lesions or nonenhancing lesions
had trace ADC values below 2 SDs of the mean of normal-appearing white matter. Other studies
showed increases in ADC values in MS lesions and perhaps also in the ADC values of normal-
appearing white matter of MS patients (,69–,73). Christiansen et al (,72) showed that the ADC values
for 39 plaques more than 4 months old (mean, 1.35 × 10-3 mm2/sec) were signi!cantly higher (P <
.01) than those for normal-appearing white matter (mean, 0.77 × 10-3 mm2/sec). Two acute MS
lesions, which were approximately 14 days old, also had elevated ADCs (mean, 1.99 × 10-3
mm2/sec). The ADCs of normal-appearing white matter in MS patients were also signi!cantly
higher than the ADCs of normal-appearing white matter in healthy volunteers (,72). Hors!eld et al
(,69) found that trace ADCs were increased in all MS lesions and that ADCs were elevated in
normal-appearing white matter in patients with a benign disease course. Scanderbeg et al (,73)
found increased water di"usion in all MS lesions compared with that of normal white matter in
control subjects.
Roychowdhury et al (,74) postulated that the decrease in ADC of homogeneously enhancing lesions
may be similar to the process in acute ischemia and postanoxic demyelination (shifts in
intracellular water protons and changes in membrane permeability may lead to decreased ADC
values). The in$ux of in$ammatory cells and associated macromolecules may also lead to
restriction of water di"usion and reduction in trace ADC. The increase in ADC is believed to be
related to the disruption of myelin, leading to an increased extracellular space (,68–,72).
Conclusions
In our experience, the signal intensity of MS lesions on DW images is variable (hyper-, iso-, or
hypointense). The majority of studies have showed increases in ADC values in MS lesions and
perhaps in the ADC values of normal-appearing white matter of MS patients (,69–,74). Therefore,
we can hypothesize that the increased intensity of MS lesions on DW images is due to the T2 shine-
through e"ect. Occasionally, the high-intensity plaques on DW images (especially homogeneously
enhancing lesions) may show reduced ADC values. Perhaps the subset of homogeneously
enhancing lesions with a low trace ADC represents a very early enhancing lesion with marked
in$ammation and no substantial demyelination (,74).
Creutzfeld-Jakob Disease
The reported cases of sporadic Creutzfeld-Jakob disease (CJD) showed high signal intensities in the
basal ganglia (putamen and caudate nucleus) and in the cortex on DW images. The high signal
intensities in the basal ganglia are also prevalent on T2-weighted and FLAIR images. The cortical
hyperintensities are usually not visualized on T2-weighted and FLAIR images (advantage of DW
imaging) (,,,,,Fig 28).
Di!erential Diagnosis of CJD and Acute Ischemic Stroke

:
In the setting of acute stroke, the high signal intensities in the basal ganglia and in the cortex on
T2-weighted SE, FLAIR, and DW images must be occasionally di"erentiated from the !ndings of CJD
(,,,,Fig 29).
•. Clinical presentation (typically acute onset in ischemic stroke).

•. ADC values (decreased in acute stroke, approximately similar to those of white matter in CJD).
Di!erential Diagnosis of CJD, Progressive Multifocal

Leukoencephalopathy, and Subacute Sclerosing Panencephalitis
(SSPE)
Progressive multifocal leukoencephalopathy (PML) is a demyelinating disease of
immunocompromised patients caused by human papovaviruses. Subacute sclerosing
panencephalitis (SSPE) occurs several years after measles infection. SSPE typically starts with
mental and behavioral abnormalities, myoclonia, tremor, and seizures. Multifocal, hyperintense
foci in white matter and the basal ganglia have been reported in PML and SSPE on T2-weighted
images (,75).
•. On T2-weighetd and FLAIR images, PML and SSPE are associated with white matter lesions,
while CJD is not.
•. The high-signal-intensity cortical lesions on DW images may be also a hallmark of CJD.

CJD is a rare, transmissible disease (caused by an agent called a “prion,” to distinguish it from a
virus) that is characterized by rapidly progressive dementia, ataxia, and myoclonus. The diagnostic
triad—progressive dementia, myoclonic jerks, and periodic sharp-wave EEG activity—may be
lacking in as many as 25%of patients. The pathologic features of CJD are microvesicular
spongiform degeneration, astrocytic glioses, and neuronal loss.
MR imaging of sporadic CJD may show high signal intensities in the basal ganglia (putamen,
caudate nucleus) and cortex. Finkenstaedt et al (,76), using T2- and proton density-weighted
images reported bilateral, symmetrically increased signal intensity in the putamen and caudate
nucleus in 79%of CJD patients, compared with just 7%of non-CJD dementia patients. More recently,
the same authors reported high signal intensities in the basal ganglia and cortex on DW images in
!ve CJD patients (,77). Increased signal intensity in the globus pallidus and thalamus on T2-
weighted images was also reported (,78).
DW imaging is more sensitive than T2- and proton density-weighted imaging in detecting cortical
abnormalities (,79). Demaerel et al also report the changing pattern of cortical involvement, with
new lesions appearing and existing lesions becoming less obvious in a short period of time (,79).
:
They suggest that patients with suspected CJD and no abnormalities on T2- and proton density-
weighted images may have cortical involvement on DW images. The reported ADC values are
normal or elevated (0.84 and 1.17 × 10-3 mm2/sec in the study of Demaerel et al [,79], 0.74–0.83 in
a case we studied (,,,,Fig 30).
In imaging variant CJD, high signal intensities are seen in the pulvinar, putamen, and caudate
nucleus on T2- and proton density-weighted SE and FLAIR images. The value of DW images in
imaging variant CJD has not been established (,80). The presumed cause of high-intensity lesions
on DW images is most probably related to the T2 shine-through e"ect, because the reported ADC
values are normal or elevated.
Conclusions
The typical presentation of sporadic CJD on MR images includes high signal intensities in the basal
ganglia (putamen, caudate nucleus) and cortex. DW imaging is more sensitive than T2- or proton
density-weighted imaging in detecting cortical abnormalities. The DW images may provide a
diagnostic clue in early detection of CJD.
Other Bright Lesions on DW Images

“
“When you’ve got a new hammer, everything looks like a nail.”
—Michael Brant-Zawadzki (,81)
Sustained Seizure Activity

DW imaging changes during seizures have been well documented in animal models but have been
rarely depicted in humans (,82). Recently, Kassem-Moussa et al reported a case of reversible
restricted water di"usibility seen on DW images early after onset of sustained seizure activity in
the absence of related T2-weighted or FLAIR imaging abnormalities (,83). Kim et al (,84) reported a
transient increase in signal intensity and swelling in the cortical gray matter, subcortical white
matter, or hippocampus on periictal T2-weighted images (in all eight patients) and on DW images
(in all !ve patients). The ADC values were reduced by 6%–28%compared with either the normal
structure opposite the lesion or in a normal control subject.
Eclampsia
:
The neuroradiologic hallmarks of eclampsia are reversible abnormalities that appear
hypoattenuating on CT studies and hyperintense on T2-weighted MR images, in a subcortical,
predominantly parietal and occipital distribution (,85,,86). In other reported cases of eclampsia, DW
images have shown these areas to have a high ADC value, suggestive of vasogenic edema (,87–,89).
Recently, Koch et al (,90) reported smaller areas of hyperintensity on DW images (suggestive of
cytotoxic edema) within predominantly hyperintense areas on T2-weighted images and
hypointense areas on DW images (suggestive of vasogenic edema).
Central Pontine Myelinolysis

Two patients with central pontine myelinolysis were studied with DW imaging 1 week after onset of
tetraplegia. In both patients, a"ected white matter showed hyperintensity on DW images,
associated with a decrease in ADC values (,91).
Caption '
:
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-$ight (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 × 10-3 mm2/sec). There is an important perfusion de!cit
(“penumbra” [,2]) in the middle cerebral artery territory.
Download as PowerPoint Open in Image Viewer
Caption '
:
Figure 1b. Acute infarction within the 1st hour after stroke. (a) Fast T2-weighted spin-echo (SE)
Caption '
:
Figure 1c. Acute infarction within the 1st hour after stroke. (a) Fast T2-weighted spin-echo (SE)
Caption '
:
Figure 1d. Acute infarction within the 1st hour after stroke. (a) Fast T2-weighted spin-echo (SE)
Caption '
:
Figure 1e. Acute infarction within the 1st hour after stroke. (a) Fast T2-weighted spin-echo (SE)
Caption '
:
Figure 1f. Acute infarction within the 1st hour after stroke. (a) Fast T2-weighted spin-echo (SE)
Caption '
:
Figure 2a. Acute infarction within the !rst 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 de!cit
and only a limited penumbra (,2).
Caption '
Figure 2b. Acute infarction within the !rst 6 hours after stroke. (a) Fast T2-weighted SE image. (b,
:
Caption '
Figure 2c. Acute infarction within the !rst 6 hours after stroke. (a) Fast T2-weighted SE image. (b,
:
Caption '
Figure 2d. Acute infarction within the !rst 6 hours after stroke. (a) Fast T2-weighted SE image. (b,
:
Caption '
Figure 2e. Acute infarction within the !rst 6 hours after stroke. (a) Fast T2-weighted SE image. (b,
:
Caption '
Figure 2f. Acute infarction within the !rst 6 hours after stroke. (a) Fast T2-weighted SE image. (b,
:
Caption '
Figure 3a. Venous infarction. (a) T2-weighted SE image and (b, c) DW echo-planar image (b) and
corresponding ADC map (c).

:
Caption '
Figure 3b. Venous infarction. (a) T2-weighted SE image and (b, c) DW echo-planar image (b) and

:
Caption '
Figure 3c. Venous infarction. (a) T2-weighted SE image and (b, c) DW echo-planar image (b) and

:
Caption '
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 !ne capsule is readily recognized.

:
Caption '
Figure 4b. Early stage of cerebral abscess. (a) T2-weighted SE image, (b) contrast-enhanced T1-

:
Caption '
Figure 4c. Early stage of cerebral abscess. (a) T2-weighted SE image, (b) contrast-enhanced T1-

:
Caption '
Figure 4d. Early stage of cerebral abscess. (a) T2-weighted SE image, (b) contrast-enhanced T1-

:
Caption '
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 ×
512 matrix). (b) Transverse T1-weighted SE image (550/14), 6-mm section thickness, three signals
averaged, one echo, and 192 × 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 !ndings
may be consistent with prominent cytotoxic edema. The di"erential diagnosis of hyperacute
arterial stroke and venous stroke remains di#cult on T2- or T1-weighed SE and DW images.

:
Caption '
Figure 5b. Acute venous infarction (superior sagittal sinus thrombosis) with high signal intensity

:
Caption '
Figure 5c. Acute venous infarction (superior sagittal sinus thrombosis) with high signal intensity

:
Caption '
Figure 5d. Acute venous infarction (superior sagittal sinus thrombosis) with high signal intensity

:
Caption '
Figure 5e. Acute venous infarction (superior sagittal sinus thrombosis) with high signal intensity

:
Caption '
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 !ndings may be
consistent with prominent vasogenic edema.

:
Caption '
Figure 6b. Acute venous infarction with low signal on DW images and increased ADC values (left

:
Caption '
Figure 6c. Acute venous infarction with low signal on DW images and increased ADC values (left

:
Caption '
Figure 6d. Acute venous infarction with low signal on DW images and increased ADC values (left

:
Caption '
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 × 512). (b) Transverse
T1-weighted nonenhanced SE image (520/14; two signals averaged; 6-mm section thickness;
matrix, 179 × 256). (c) Transverse T1-weighted contrast-enhanced SE image (520/14; two signals
averaged; 6-mm section thickness; matrix, 179 × 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 $uid 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 e"ect). On DW images (e), the peritumoral vasogenic edema is
isointense to the white matter because the e"ect of increased di"usion (dark) is compensated for
by the increased T2 values of edema (bright). The peritumoral edema, cerebrospinal $uid, and
necrotic component of the tumor are hyperintense (high di"usion) on the ADC map.
:
Caption '
Figure 7b. Glioblastoma multiforme. (a) Transverse T2-weighted fast SE image (5000/128; two
:
Caption '
Figure 7c. Glioblastoma multiforme. (a) Transverse T2-weighted fast SE image (5000/128; two
:
Caption '
Figure 7d. Glioblastoma multiforme. (a) Transverse T2-weighted fast SE image (5000/128; two
:
Caption '
:
Caption '
Figure 7e. Glioblastoma multiforme. (a) Transverse T2-weighted fast SE image (5000/128; two

:
Caption '
Figure 7f. Glioblastoma multiforme. (a) Transverse T2-weighted fast SE image (5000/128; two
:
Caption '
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.

:
Caption '
Figure 8b. Multiple metastases. (a) Axial T2-weighted fast SE, (b, c) T1-weighted (b) nonenhanced

:
Caption '
Figure 8c. Multiple metastases. (a) Axial T2-weighted fast SE, (b, c) T1-weighted (b) nonenhanced

:
Caption '
Figure 8d. Multiple metastases. (a) Axial T2-weighted fast SE, (b, c) T1-weighted (b) nonenhanced

:
Caption '
Figure 8e. Multiple metastases. (a) Axial T2-weighted fast SE, (b, c) T1-weighted (b) nonenhanced

:
Caption '
Figure 9a. Multiple metastases in same patient as in ,,,,,,Figure 8, at a di"erent level. (a) Axial T2-
weighted fast SE, (b, c) T1-weighted (b) nonenhanced and (c) contrast-enhanced SE, and (d) DW
images (trace) and (e) corresponding ADC map. (f) Magni!cation of e. The ADC value for region of
interest 1 (solid component of metastasis) is 0.76 × 10-3 mm2/sec; for region of interest 2
(contralateral gray and white matter), the ADC value is 0.73 × 10-3 mm2/sec.

:
Caption '
Figure 9b. Multiple metastases in same patient as in ,,,,,,Figure 8, at a di"erent level. (a) Axial T2-

:
Caption '
Figure 9c. Multiple metastases in same patient as in ,,,,,,Figure 8, at a di"erent level. (a) Axial T2-

:
Caption '
Figure 9d. Multiple metastases in same patient as in ,,,,,,Figure 8, at a di"erent level. (a) Axial T2-

:
Caption '
Figure 9e. Multiple metastases in same patient as in ,,,,,,Figure 8, at a di"erent level. (a) Axial T2-

:
Caption '
Figure 9f. Multiple metastases in same patient as in ,,,,,,Figure 8, at a di"erent level. (a) Axial T2-

:
Caption '
Figure 10a. Cerebral metastasis. (a) T2-weighted fast SE, (b) contrast-enhanced T1-weighted SE,
and (c) DW (sensitizing direction = z) multishot echo-planar (800/123, !ve signals averaged, 6-mm
section thickness images and (d) corresponding ADC map.

:
Caption '
Figure 10b. Cerebral metastasis. (a) T2-weighted fast SE, (b) contrast-enhanced T1-weighted SE,

:
Caption '
Figure 10c. Cerebral metastasis. (a) T2-weighted fast SE, (b) contrast-enhanced T1-weighted SE,

:
Caption '
Figure 10d. Cerebral metastasis. (a) T2-weighted fast SE, (b) contrast-enhanced T1-weighted SE,

:
Caption '
Figure 11a. Cerebral metastasis with increased signal intensity on DW images. (a) Axial T2-
(trace) images and (e) corresponding ADC map. Old hemorrhagic content was found at surgery.

:
Caption '
Figure 11b. Cerebral metastasis with increased signal intensity on DW images. (a) Axial T2-

:
Caption '
Figure 11c. Cerebral metastasis with increased signal intensity on DW images. (a) Axial T2-

:
Caption '
Figure 11d. Cerebral metastasis with increased signal intensity on DW images. (a) Axial T2-

:
Caption '
Figure 11e. Cerebral metastasis with increased signal intensity on DW images. (a) Axial T2-

:
Caption '
Figure 12a. Benign meningioma. (a) T2-weighted SE, (b) T1-weighted SE, and (c) multishot
(800/123, one signal acquired, 6-mm section thickness) DW echo-planar (sensitizing direction = z)
images and (d) corresponding ADC map. (e, f) Contrast-enhanced T1-weighted SE images acquired
in the (e) transverse and (f) coronal planes. This meningioma is hyperintense on the DW echo-
planar image and iso- to hypointense on the corresponding ADC map. The ADC values were in the
range 0.39-0.46 × 10-3 mm2/sec (0.61-0.63 × 10-3 mm2/sec for the contralateral white and gray
matter).

:
Caption '
Figure 12b. Benign meningioma. (a) T2-weighted SE, (b) T1-weighted SE, and (c) multishot
matter).

:
Caption '
Figure 12c. Benign meningioma. (a) T2-weighted SE, (b) T1-weighted SE, and (c) multishot
matter).

:
Caption '
Figure 12d. Benign meningioma. (a) T2-weighted SE, (b) T1-weighted SE, and (c) multishot
matter).

:
Caption '
Figure 12e. Benign meningioma. (a) T2-weighted SE, (b) T1-weighted SE, and (c) multishot
matter).

:
Caption '
Figure 12f. Benign meningioma. (a) T2-weighted SE, (b) T1-weighted SE, and (c) multishot
matter).

:
Caption '
Figure 13a. Calci!ed meningioma with cortical infarction. (a) Nonenhanced CT, (b) T2-weighted
SE, (c) contrast-enhanced T1-weighted SE, and (d) multishot (800/123, one signal acquired, 6-mm
section thickness) DW echo-planar (sensitizing direction = z) images and (e) corresponding ADC
map. This calci!ed meningioma was an incidental !nding. It is hypointense on the DW echo-planar
image and on the corresponding ADC map. The ADC values were in the range 0.21-0.75 × 10-3
mm2/sec.

:
Caption '
Figure 13b. Calci!ed meningioma with cortical infarction. (a) Nonenhanced CT, (b) T2-weighted
mm2/sec.

:
Caption '
Figure 13c. Calci!ed meningioma with cortical infarction. (a) Nonenhanced CT, (b) T2-weighted SE,
(c) contrast-enhanced T1-weighted SE, and (d) multishot (800/123, one signal acquired, 6-mm
mm2/sec.

:
Caption '
Figure 13d. Calci!ed meningioma with cortical infarction. (a) Nonenhanced CT, (b) T2-weighted
mm2/sec.

:
Caption '
Figure 13e. Calci!ed meningioma with cortical infarction. (a) Nonenhanced CT, (b) T2-weighted
mm2/sec.

:
Caption '
Figure 14a. Cerebral lymphoma. (a) Axial T2-weighted fast SE (5000/128; two signals averaged; 6-
mm section thickness; echo train length, 23; matrix, 230 × 512), (b) axial T1-weighted nonenhanced
SE (520/14, two signals averaged, 6-mm section thickness, 179 × 256 matrix), (c) axial T1-weighted
contrast-enhanced SE (520/14, two signals averaged, 6-mm section thickness, 179 × 256), and (d)
axial DW echo-planar (sensitizing direction = z) (800/123, one signal acquired, 6-mm section
thickness) images and (e) corresponding ADC map. The enhancing component shows high signal
intensity on the DW echo-planar image (d) and reduced ADC values (e). The peritumoral edema is
hyperintense on the ADC map.

:
Caption '
Figure 14b. Cerebral lymphoma. (a) Axial T2-weighted fast SE (5000/128; two signals averaged; 6-

:
Caption '
Figure 14c. Cerebral lymphoma. (a) Axial T2-weighted fast SE (5000/128; two signals averaged; 6-

:
Caption '
Figure 14d. Cerebral lymphoma. (a) Axial T2-weighted fast SE (5000/128; two signals averaged; 6-

:
Caption '
Figure 14e. Cerebral lymphoma. (a) Axial T2-weighted fast SE (5000/128; two signals averaged; 6-

:
Caption '
Figure 15a. Cerebral lymphoma with hyperintense and hypointense components on DW images.
(a) T2-weighted fast SE, (b) contrast-enhanced T1-weighted SE, and (c) DW (trace) multishot echo-
planar images and (d) corresponding ADC map. The central component of lymphoma in c shows
peripheral hyperintensity and central hypointensity (due to necrosis?).

:
Caption '
Figure 15b. Cerebral lymphoma with hyperintense and hypointense components on DW images.

:
Caption '
Figure 15c. Cerebral lymphoma with hyperintense and hypointense components on DW images.

:
Caption '
Figure 15d. Cerebral lymphoma with hyperintense and hypointense components on DW images.

:
Caption '
Figure 16a. Cerebral lymphoma with hyperintense and hypointense components on DW images
(same case as ,,,,,Fig 15 but di"erent level). (a) T2-weighted fast SE, (b) contrast-enhanced T1-
weighted SE, and (c) DW (trace) multishot echo-planar images and (d) corresponding ADC map.

:
Caption '
Figure 16b. Cerebral lymphoma with hyperintense and hypointense components on DW images

:
Caption '
Figure 16c. Cerebral lymphoma with hyperintense and hypointense components on DW images

:
Caption '
Figure 16d. Cerebral lymphoma with hyperintense and hypointense components on DW images

:
Caption '
Figure 17a. Epidermoid cyst. (a) Axial T2-weighted, (b) T1-weighted SE, and (c) corresponding DW
images (trace) and (d) ADC map show typical high signal intensity of epidermoid cyst on DW
images (c) and isointensity with white and gray matter on ADC maps (d).

:
Caption '
Figure 17b. Epidermoid cyst. (a) Axial T2-weighted, (b) T1-weighted SE, and (c) corresponding DW

:
Caption '
Figure 17c. Epidermoid cyst. (a) Axial T2-weighted, (b) T1-weighted SE, and (c) corresponding DW

:
Caption '
Figure 17d. Epidermoid cyst. (a) Axial T2-weighted, (b) T1-weighted SE, and (c) corresponding DW

:
Caption '
Figure 18a. Arachnoid cyst plus meningioma. (a) Axial T2-weighted, (b) contrast-enhanced T1-
weighted SE, and (c) corresponding DW images (sensitizing direction = z) and (d) ADC (trace) map.
The arachnoid cyst has typical low signal intensity on the DW image (c) and isointensity with CSF on
the ADC map (d).

:
Caption '
Figure 18b. Arachnoid cyst plus meningioma. (a) Axial T2-weighted, (b) contrast-enhanced T1-
the ADC map (d).

:
Caption '
Figure 18c. Arachnoid cyst plus meningioma. (a) Axial T2-weighted, (b) contrast-enhanced T1-
the ADC map (d).

:
Caption '
Figure 18d. Arachnoid cyst plus meningioma. (a) Axial T2-weighted, (b) contrast-enhanced T1-
the ADC map (d).

:
Caption '
Figure 19a. Cerebral abscess (Streptococcus intermedius, Fusobacterium nucleatum and Actinomyces
meyeri). (a) Axial T2-weighted fast SE (5300/128; two signals averaged; 6-mm section thickness;
echo train length, 23; matrix, 230 × 512), (b) axial T1-weighted contrast-enhanced SE (580/14, two
signals averaged, 6-mm section thickness, 192 × 256 matrix), and (c) axial DW (sensitizing direction
= x) multishot echo-planar (800/123, one signal acquired, 6-mm section thickness) images and (d)
corresponding ADC map.

:
Caption '
Figure 19b. Cerebral abscess (Streptococcus intermedius, Fusobacterium nucleatum and Actinomyces

:
Caption '
Figure 19c. Cerebral abscess (Streptococcus intermedius, Fusobacterium nucleatum and Actinomyces

:
Caption '
Figure 19d. Cerebral abscess (Streptococcus intermedius, Fusobacterium nucleatum and Actinomyces

:
Caption '
Figure 20a. Glioblastoma multiforme. On (a) T2-weighted fast SE and (b) contrast-enhanced T1-
weighted SE images, the di"erential diagnosis of glioblastoma and abscess is impossible. (c) DW
(sensitizing direction = z) multishot echo-planar image (800/123, !ve signals averaged, 6-mm
section thickness) and (d) corresponding ADC map show central hypointensity on DW image and
hyperintensity on ADC map, consistent with the diagnosis of tumor.

:
Caption '
Figure 20b. Glioblastoma multiforme. On (a) T2-weighted fast SE and (b) contrast-enhanced T1-

:
Caption '
Figure 20c. Glioblastoma multiforme. On (a) T2-weighted fast SE and (b) contrast-enhanced T1-

:
Caption '
Figure 20d. Glioblastoma multiforme. On (a) T2-weighted fast SE and (b) contrast-enhanced T1-

:
Caption '
Figure 21a. Multiple Tbc granulomas. (a) Axial T2-weighted fast SE, (b) FLAIR, (c) contrast-
enhanced T1-weighted SE, and (d) DW (sensitizing direction = z) images and (e) corresponding ADC
map. Some of the granulomas show high signal intensity on DW images (c), but ADC values are
similar to those of white matter.

:
Caption '
Figure 21b. Multiple Tbc granulomas. (a) Axial T2-weighted fast SE, (b) FLAIR, (c) contrast-

:
Caption '
Figure 21c. Multiple Tbc granulomas. (a) Axial T2-weighted fast SE, (b) FLAIR, (c) contrast-

:
Caption '
Figure 21d. Multiple Tbc granulomas. (a) Axial T2-weighted fast SE, (b) FLAIR, (c) contrast-

:
Caption '
Figure 21e. Multiple Tbc granulomas. (a) Axial T2-weighted fast SE, (b) FLAIR, (c) contrast-

:
Caption '
Figure 22a. Cerebral metastases. (a) Axial T2-weighted fast SE, (b, c) T1-weighted (b)
nonenhanced and (c) contrast-enhanced SE, and (d) DW (sensitizing direction = z) images and (e)
corresponding ADC map. These multiple metastases of a small-cell lung carcinoma had high
cellularity at histologic study.

:
Caption '
Figure 22b. Cerebral metastases. (a) Axial T2-weighted fast SE, (b, c) T1-weighted (b)

:
Caption '
Figure 22c. Cerebral metastases. (a) Axial T2-weighted fast SE, (b, c) T1-weighted (b)

:
Caption '
Figure 22d. Cerebral metastases. (a) Axial T2-weighted fast SE, (b, c) T1-weighted (b)

:
Caption '
Figure 22e. Cerebral metastases. (a) Axial T2-weighted fast SE, (b, c) T1-weighted (b)

:
Caption '
Figure 23a. Cerebral metastases (same case as Fig 22 but di"erent level). (a) Axial T2-weighted
fast SE, (b, c) T1-weighted (b) nonenhanced and (c) contrast-enhanced SE, and (d) DW (sensitizing
direction = z) images and (e) corresponding ADC map.

:
Caption '
Figure 23b. Cerebral metastases (same case as Fig 22 but di"erent level). (a) Axial T2-weighted

:
Caption '
Figure 23c. Cerebral metastases (same case as Fig 22 but di"erent level). (a) Axial T2-weighted

:
Caption '
Figure 23d. Cerebral metastases (same case as Fig 22 but di"erent level). (a) Axial T2-weighted

:
Caption '
Figure 23e. Cerebral metastases (same case as Fig 22 but di"erent level). (a) Axial T2-weighted

:
Caption '
Figure 24a. Herpes encephalitis. (a) Axial T2-weighted fast SE (5400/90, one signal acquired, 6-mm
section thickness, one echo, 192 × 256 matrix), (b) axial T1-weighted nonenhanced SE (580/14, two
signals averaged, 6-mm section thickness), and (c) axial T1-weighted contrast-enhanced (580/14,
two signals averaged, 6-mm section thickness) images. On the T2-weighted SE image,
heterogeneous hyperintense lesions (arrows) are seen in the temporal and hippocampal areas. On
the nonenhanced T1-weighted SE image, less extensive hyperintense areas (hemorrhages) can also
be recognized (arrow). After gadolinium injection, asymmetric, gyriform enhancement is seen in
the temporal lobes (arrow) and cingulate gyrus, characteristic of herpes encephalitis.

:
Caption '
Figure 24b. Herpes encephalitis. (a) Axial T2-weighted fast SE (5400/90, one signal acquired, 6-mm

:
Caption '
Figure 24c. Herpes encephalitis. (a) Axial T2-weighted fast SE (5400/90, one signal acquired, 6-mm

:
Caption '
Figure 25a. Hyperacute hemorrhage (4 hours after onset). (a) T2- and (b) T1-weighted SE and (c)
DW (sensitizing direction = z) multishot echo-planar images and (d) corresponding ADC map.

:
Caption '
Figure 25b. Hyperacute hemorrhage (4 hours after onset). (a) T2- and (b) T1-weighted SE and (c)

:
Caption '
Figure 25c. Hyperacute hemorrhage (4 hours after onset). (a) T2- and (b) T1-weighted SE and (c)

:
Caption '
Figure 25d. Hyperacute hemorrhage (4 hours after onset). (a) T2- and (b) T1-weighted SE and (c)

:
Caption '
Figure 26a. Late subacute stage hemmorhage (27 days after onset). (a) T2- and (b) T1-weighted SE
and (c) DW (trace) multishot echo-planar images and (d) corresponding ADC map.

:
Caption '
Figure 26b. Late subacute stage hemmorhage (27 days after onset). (a) T2- and (b) T1-weighted SE

:
Caption '
Figure 26c. Late subacute stage hemmorhage (27 days after onset). (a) T2- and (b) T1-weighted SE

:
Caption '
Figure 26d. Late subacute stage hemmorhage (27 days after onset). (a) T2- and (b) T1-weighted SE

:
Caption '
Figure 27a. Multiple sclerosis, with recent hypoesthesia in the left lower limb. (a) Axial T2-
weighted fast SE (5000/128; two signals averaged; 6-mm section thickness; echo train length, 23;
matrix, 230 × 512), (b) axial fast FLAIR (6000/105, 2200-msec inversion time, two signals averaged,
6-mm section thickness, 182 × 256 matrix), (c) axial T1-weighted contrast-enhanced SE (540/14, two
signals averaged, 6-mm section thickness, 230 × 512 matrix) images. (d) Axial DW (sensitizing
direction = x) multishot echo-planar image (800/123, one signal acquired, 6-mm section thickness)
and (e) corresponding ADC map. (f) Axial DW (sensitizing direction = z) multishot echo-planar
image and (g) corresponding ADC map. Active plaque is seen with contrast enhancement (c). Two
additional small plaques are recognized on the FLAIR iamge (b). The ADC values of active plaque
are increased; however, depending on the orientation of the corticospinal !bers, the conspicuity
may be lower with respect to conventional sequences. This homogeneously enhancing lesion
shows high signal intensity on DW images (d, f) and increased ADC values (e, g). The small,
nonenhancing plaques are not recognized on the DW images and ADC maps.
:
Caption '
Figure 27b. Multiple sclerosis, with recent hypoesthesia in the left lower limb. (a) Axial T2-
:
Caption '
Figure 27c. Multiple sclerosis, with recent hypoesthesia in the left lower limb. (a) Axial T2-
:
Caption '
Figure 27d. Multiple sclerosis, with recent hypoesthesia in the left lower limb. (a) Axial T2-
:
Caption '
:
Caption '
Figure 27e. Multiple sclerosis, with recent hypoesthesia in the left lower limb. (a) Axial T2-

:
Caption '
Figure 27f. Multiple sclerosis, with recent hypoesthesia in the left lower limb. (a) Axial T2-weighted
fast SE (5000/128; two signals averaged; 6-mm section thickness; echo train length, 23; matrix, 230
× 512), (b) axial fast FLAIR (6000/105, 2200-msec inversion time, two signals averaged, 6-mm
section thickness, 182 × 256 matrix), (c) axial T1-weighted contrast-enhanced SE (540/14, two
:
Caption '
Figure 27g. Multiple sclerosis, with recent hypoesthesia in the left lower limb. (a) Axial T2-
:
Caption '
Figure 28a. CJD. (a) Axial T2-weighted SE, (b) FLAIR and (c) DW echo-planar images. The
hyperintensity of the caudate nuclei is obvious on the FLAIR and DW images. The left occipital
cortical involvement is best appreciated on the DW image. (d) Histology specimen shows
astrogliosis and microvesicular spongiform degeneration. (All images courtesy of Philippe
Demaerel, MD, University Hospitals, Leuven, Belgium.)
:
Caption '
Figure 28b. CJD. (a) Axial T2-weighted SE, (b) FLAIR and (c) DW echo-planar images. The

:
Caption '
Figure 28c. CJD. (a) Axial T2-weighted SE, (b) FLAIR and (c) DW echo-planar images. The

:
Caption '
Figure 28d. CJD. (a) Axial T2-weighted SE, (b) FLAIR and (c) DW echo-planar images. The

:
Caption '
Figure 29a. Acute stroke 4 hours after onset. (a) Axial T2-weighted fast SE (5000/128; two signals
averaged; 6-mm section thickness; echo train length, 23; matrix, 230 × 512), (b) axial fast FLAIR
(6000/105, 2200-msec inversion time, two signals averaged, 6-mm section thickness, 182 × 256
matrix), and (c) axial DW (sensitizing direction = z) multishot echo-planar (800/123, one signal
acquired, 6-mm section thickness) images. The cortical involvement of acute stroke (arrow, c) looks
similar to the cortical hyperintensities of CJD.

:
Caption '
Figure 29b. Acute stroke 4 hours after onset. (a) Axial T2-weighted fast SE (5000/128; two signals

:
Caption '
Figure 29c. Acute stroke 4 hours after onset. (a) Axial T2-weighted fast SE (5000/128; two signals

:
Caption '
Figure 30a. CJD. (a) ADC values for the abnormal area (roi 1) and normal appearing contralateral
side (roi 2), (b) DW image shows striking hyperintensity of caudate nucleus and cortex. (c)
Corresponding ADC map shows the two areas of interest.

:
Caption '
Figure 30b. CJD. (a) ADC values for the abnormal area (roi 1) and normal appearing contralateral

:
Caption '
Figure 30c. CJD. (a) ADC values for the abnormal area (roi 1) and normal appearing contralateral
TABLE 1. ADC Values (× 10-3 mm2/sec) of Ischemic Lesions during Di!erent Time Intervals
:
Note.—NA = not available.
TABLE 2. Signal Intensity of Solid Portion of Gliomas on DW Images and Their ADC Values
*Some gliomas showed mixed intensity, so the total percentage exceeds 100%.
TABLE 3. Signal Intensity of Meningiomas on DW Images and Their Relative ADC Values
*Some meningiomas showed mixed intensity, so the total percentage exceeds 100%.
TABLE 4. Cyst Appearance with Di!erent MR Imaging Sequences

:
TABLE 5. Signal Intensity with Di!erent Sequences and Reported ADC Values for Di!erent
Stages of Hemorrhage
*Mean value × 10-3 mm2/sec.
TABLE 6. ADC values of Hyperacute Hematomas during Di!erent Time Intervals
Abbreviation: ADC = apparent di"usion coe#cient, CISS = constructive interference in the steady
state, DW = di"usion-weighted, FLAIR = $uid-attenuated inversion recovery, SE = spin echo, TOF =
time of $ight.
The authors express their gratitude to Eddy Broodtaers, Filip De Ridder, and Walter Rijsselaere for
their excellent technical support.
Article History
Published in print: Jan 2003
We recommend
Diffusion-weighted MR Imaging of Early-Stage Creutzfeldt-Jakob Disease: Typical and Atypical Manifestations

:
Ryutarou Ukisu et al., Radiographics, 2006
Initial Ischemic Event: Perfusion-weighted MR Imaging and Apparent Diffusion Coefficient for Stroke Evolution
Rüdiger J. Seitz et al., Radiology, 2005
MR diffusion imaging in stroke: review and controversies.

N J Beauchamp et al., Radiographics, 1998
Cortical Linear Lesions in Wernicke’s Encephalopathy: Can Diffusion-Weighted Imaging Herald Prognostic
Information?
Álvaro Machado, M.D. et al., J Neuropsychiatry Clin Neurosci, 2010
Cerebellar Infarct
Kimon Ioannides et al., StatPearls, 2021
G57(P) To present a case of perinatal arterial ischaemic stroke (PAIS) that presented with recurrent focal
seizures at birth
A Sharma et al., Archives of Disease in Childhood, 2020
Powered by
820 Jorie Blvd., Suite 200

Oak Brook, IL 60523-2251
U.S. & Canada: 1-877-776-2636
Outside U.S. & Canada: 1-630-571-7873
Terms of Use
© 2021 Radiological Society of North America
:

Imaging Tutorial - Differential Diagnosis of Bright Lesions On Diffusion-Weighted MR Images - RadioGraphics

Uploaded by

Document Information

Original Title

Copyright

Available Formats

Share this document

Share or Embed Document

Sharing Options

Did you find this document useful?

Is this content inappropriate?

Copyright:

Available Formats

Imaging Tutorial - Differential Diagnosis of Bright Lesions On Diffusion-Weighted MR Images - RadioGraphics

Uploaded by

Copyright:

Available Formats

!

Home > RadioGraphics > Vol. 23, No. 1

Online Only & Free Access

Imaging Tutorial: Di!erential Diagnosis of Bright

' Author A"liations

Published Online: Jan 1 2003https://doi.org/10.1148/rg.e7

Basic Physics of Di!usion-weighted (DW) Magnetic

Typical Presentation on DW Images and Apparent Di!usion

Di!erential Diagnosis with Venous Stroke

Hints for di!erential diagnosis:

Di!erential Diagnosis with Cerebritis

Hints for di!erential diagnosis:

•. See the section on In!ammation: Abscess.

Background and Discussion

Di!erential Diagnosis with Arterial Stroke

For more information, see the section on Acute Infarction.

Background and Discussion

Presumed Causes of Low and High Signal Intensity on DW Images

Typical Presentation on DW Images and ADC Maps

Di!erential Diagnosis of Ring-enhancing Cerebral Masses

For more information, see the section on In$ammation: Abscess.

Background and Discussion

Can the ADC Values Di!erentiate between Di!erent Grades of Gliomas?

In our experience, the signal intensity of nonnecrotic components of metastases on DW images is

Di!erential Diagnosis of Ring-enhancing Cerebral Masses

For more information, see the section on In$ammation: Abscess

Background and Discussion

In our experience, the signal intensity of nonnecrotic components of metastases on DW images is

Tumor cellularity is probably a major determinant of signal intensity of solid components of

Background and Discussion

Hints for di!erential diagnosis:

Background and Discussion

Tumors: Epidermoid Cyst

Di!erential Diagnosis with Arachnoid Cyst

Hints for di!erential diagnosis:

Background and Discussion

Di!erential Diagnosis of Abscess and Acute Ischemic Stroke

•. Clinical presentation (typically acute onset in ischemic stroke).

Di!erential Diagnosis of Abscess and Cystic or Necrotic Tumors

Hints for di!erential diagnosis:

Background and Discussion

Presumed Causes of High Signal Intensity on DW Images

Typical Presentation on DW Images and ADC Maps

Di!erential Diagnosis of Granulomas and Nodular Cerebral

Typical Presentation on DW Images and ADC Maps

Hints for di!erential diagnosis herpes encephalitis versus ischemic stroke:

•. Clinical presentation (acute onset in ischemic stroke, more progressive in herpes

Typical Presentation on DW Images and ADC Maps

Di!erential Diagnosis with Hyperacute Ischemic Stroke

Hints for di!erential diagnosis:

•. In hyperacute ischemic stroke the T2-weighted SE and T2*-weighted gradient-echo "ndings

Background and Discussion

Hyperacute Stage (intracellular oxyhemoglobin)

1. A shrinkage of the extracellular space with clot retraction (,63).

Late Subacute Stage (extracellular methemoglobin)

Typical Presentation on DW Images and ADC Maps

Background and Discussion

Di!erential Diagnosis of CJD and Acute Ischemic Stroke

Hints for di!erential diagnosis:

•. Clinical presentation (typically acute onset in ischemic stroke).

Di!erential Diagnosis of CJD, Progressive Multifocal

Hints for di!erential diagnosis:

Background and Discussion