Health&Medicine.

1. Radiological application of diffusion-
weighted images in Neuroradiology.
Dr/ ABD ALLAH NAZEER. MD.

2. A relatively large number of intracranial diseases can
show restricted diffusion and may therefore appear
bright on diffusion-weighted images. An incomplete
listing by category of disease is shown below, with
the most common examples highlighted in red:
Restricted Diffusion.
Which diseases are "bright" on DW imaging and why?

4. Diffusion weighted MRI in acute stroke.
Diffusion weighted imaging (DWI) is a commonly performed
MRI sequence for evaluation of acute ischemic stroke and is
sensitive in the detection of small and early infarcts.
Conventional MRI sequences (T1WI, T2WI) may not
demonstrate an infarct for 6 hours, and small infarcts may
be hard to appreciate on CT for days, especially without the
benefit of prior imaging.
Increased DWI signal in ischemic brain tissue is observed
within a few minutes after arterial occlusion and progresses
through a stereotypic sequence of apparent diffusion
coefficient (ADC) reduction, followed by subsequent increase,
pseudo-normalization and, finally, permanent
elevation. Reported sensitivity ranges from 88-100% and
specificity ranges from 86-100%.

5. Diffusion-weighted imaging (DWI) has become a pillar of current
neuroimaging and has revolutionized stroke imaging since its introduction
in the mid-1980s.
DWI provides image contrast that is dependent on the molecular motion
of water.
Diffusion abnormalities represent alterations in the random movement
of water molecules in tissues, revealing their micro architecture, and
occur in many neurological conditions1.
In a DWI sequence diffusion sensitization gradients are applied on either
side of the 180° refocusing pulse. The parameter “b value” decides the
diffusion weighting and is expressed in s/mm. It is proportional to the
square of the amplitude and duration of the gradient applied.
Diffusion is qualitatively evaluated on trace images and quantitatively by
the parameter called apparent diffusion coefficient (ADC). Tissues with
restricted diffusion are bright on the trace image and hypointense on the
ADC map.
In the brain, factors contributing to the measured ADC include true random
diffusion, tortuosity of the diffusion space, cytosolic streaming, exchange
times between compartments and restriction by cell membranes.

6. Radiographic features
The appearance of DWI/ADC depends on the timing.
Acute (0-7 days)
ADC value decreases with maximal signal reduction at 1 to 4 days
marked hyperintensity on DWI (a combination of T2 and diffusion weighting), less
hyperintensity on exponential images, and hypointensity on ADC images
subsequently, release of inflammatory mediators from ischemic brain tissue leads to
vasogenic edema with extravasation of water molecules from blood vessels to
expand the interstitial space, where water molecule diffusion is highly unrestricted
early DWI reversal (aka diffusion lesion reversal) can occur, most frequently with
reperfusion, but this rarely alters the size of the eventual infarct and is probably
a 'pseudoreversal.
Subacute (1-3 weeks)
ADC pseudonormalization occurs in the second week (7-15 days)
ADC values rise and return to near baseline
irreversible tissue necrosis is present despite normal ADC values
DWI remains hyperintense due to T2 shine through
after 2 weeks ADC values continue to rise above normal parenchyma and the region
appears hyperintense
Chronic (>3 weeks)
ADC signal high
DWI signal low (as T2 hyperintensity and thus T2 shine through resolve)

7. 1.Increase in intracellular water. With cell death or
insufficient intracellular energy metabolism, membrane
pumps responsible for maintaining ionic gradients fail and
swelling (cytotoxic edema) develops.
2.Reduction in extracellular space. This occurs as a
consequence of cellular swelling, resulting in increased
tortuosity of extracellular pathways.
3.Fragmentation of cellular components. With cell death or
rupture, cellular components (membranes, mitochondria,
endoplasmic reticulum, proteins, etc) dissociate, fragment,
and unravel. Both intracellular and extracellular viscosity
increases.
Cerebral Infarction
Restricted diffusion typically occurs within 30-120 minutes
after a cerebral infarction, returning to normal by 10-14
days. The principal mechanisms are thought to be:

8. Acute stroke. a Increased signal intensity on DWI in the territory of the right middle
cerebral artery (MCA), which corresponds to an area of low ADC value in b (asterisks),
representing the extension of an acute ischaemic stroke. c A clot as the etiology,
presenting as a linear hypointense abnormality in the MCA on T2*WI (arrow)

9. Images of a newborn with seizures at 6 h of age. MRI of the brain performed on day 3 of
life. a Axial T2-W image shows large left middle cerebral artery territory infarction with loss
of the cortical ribbon (arrows). b, c DW image (b) and ADC map (c) show decreased diffusion
throughout the left middle cerebral artery territory as well as in the left thalamus (asterisk)

10. Acute left MCA
territory infarct
secondary to left ICA
dissection. Axial DWI
(A) & ADC (B) images
of brain demonstrate
acute infarct in left
MCA territory (red &
white arrows). On
axial T2W image (C),
hyperintense crescent
(green arrow) with a
medially located string
like flow void in left
ICA suggesting
dissection with
thrombosis of the false
lumen. On MIP
reconstruction of 3D
TOF angiogram (D)
loss of flow related
signal in left MCA
(yellow arrow) and ICA
is visualized (blue
arrow) suggesting
thrombosis.

11. Basilar artery dissection with acute infarcts in bilateral cerebellar hemispheres. Axial DWI image of brain (A) and corresponding
ADC map (B)demonstrate acute infarcts in bilateral cerebellar lobes and middle cerebellar peduncles (*). On 3D TOF MR angiogram
(C) there is a hypointense flap (red arrow)at the basilar artery suggesting basilar artery dissection. On CT angiogram (D) and
3D VRT image (E) the dissecting flap in the basilar artery (red arrows) and luminal narrowing can be well appreciated.

12. Suspected vasculitis. Malignant right ICA territory infarct.

13. 15 years old with superior sagittal sinus thrombosis. Acute venous infarcts showing diffusion restriction in bilateral frontal lobes.

14. Diffuse axonal injury (DAI) and cortical contusions
constitute the vast majority of primary intra-axial
lesions in cases of traumatic brain injury and are
associated with significant morbidity. DAI results
from rotational acceleration and deceleration
forces producing diffuse shear-strain
deformations of brain tissue, usually at the gray-
white junction, in the corpus callosum, and at the
dorsolateral aspect of the upper brain stem.
Cortical contusions are caused by direct contact
between the skull and brain parenchyma, most
often in the temporal and frontal lobes.

15. 52 year-old man with intracranial
injuries sustained in a motor vehicle
accident. Brain MR imaging was
performed 18 days after the
accident.
A and B, Axial fast spin-echo T2-
weighted (4000/98/1) (A) and
FLAIR (11000/125/1) (B) images
both show evidence of diffuse
axonal injury, as evidenced by
hyperintense signal in the splenium.
C and D, Isotropic diffusion-
weighted (10000/125/1) (C) and
diffusion trace (D) images show
hyperintense signal and decreased
ADC values, respectively, consistent
with cellular edema. Of particular
interest in this case is that ADC
values were decreased well into the
subacute period after the injury.

16. 40 year-old man examined
with brain MR imaging 7
days after injury.
A and B, Axial fast spin-
echo (4000/98/1) (A) and
FLAIR (11000/125/1) (B)
images at the level of the
splenium confirm diffuse
axonal injury, with
hyperintense signal seen
on both pulse sequences.
Also note the small
bilateral frontal subdural
hematomas and a small
contusion in the left
anterior temporal lobe.
C and D, Isotropic
diffusion-weighted
(10000/125/1) (C) and
diffusion trace (D) images
show hyperintense signal
and decreased ADC
values, respectively.

17. Bifrontal traumatic
microbleeds (TMBs) are
identified on head CT (A).
Gradient-echo MRI (B)
reveals additional TMBs
involving the forceps
minor fibers and the
splenium of the corpus
callosum. Diffusion-
weighted MRI (C) and
apparent diffusion
coefficient map (D)
demonstrate restricted
diffusion in the genu of
the corpus callosum
extending into the
bifrontal white matter.

26. Spinal cord ischemia. High T2 signal abnormality in the conus medullaris with
diffusion restriction on DWI (arrows) compatible with an ischaemic lesion

27. Arterial dissection. DWI
(a), ADC (b), non-
contrast FAT SAT T1 (c)
and coronal MIP
reconstruction of the
basilar artery (d)
demonstrate a
dissection with mural
hematoma represented
by the “crescent sign”
(arrows), which shows
restricted diffusion and
hyperintensity on T1WI

28. Venous thrombosis. DWI (a), ADC map (b) and sagittal reconstruction of T1 3D with
gadolinium (c) show thrombosis of the left jugular vein (arrows), presenting with
restricted diffusion and a filling defect in the vessel after contrast administration.

31. Parechovirus encephalitis. Neonate with seizures DWI images
demonstrates extensive and symmetric areas of diffusion restriction
involving periventricular white matter, corpus callosum and thalamus.

32. Rota viral encephalitis. 5day old child with seizures. DWI images demonstrates extensive and symmetric
areas of diffusion restriction involving periventricular white matter, corpus callosum and thalamus.

33. Dengue encephalitis. 4-year old child with fever since 4 days,1 episode of seizure, altered sensorium. MR imaging demonstrates bilateral
symmetrical T2/FLAIR hyperintensity (A,B) and T1 hypointensity(C) in thalamus, posterior limb of internal capsules. The corresponding
areas demonstrate restricted diffusion (D,E) with blooming(F)seen in bilateral thalamus suggestive of hemorrhage. Serology was positive
for Dengue. Imaging differential for this appearance could be Acute necrotizing encephalitis of childhood.

34. 18 years old with Japanese encephalitis. T2/FLAIR hyperintensities seen in bilateral thalami and substantia nigra
with areas of diffusion restriction. Associated right frontal neurocysticercosis(NCC) with perifocal edema can be
noted. NCC and JE co-infection can be attributed to common epidemiologic and socio-demographic factors.

35. 17 years old with Influenza encephalitis, presenting as transient splenial lesion.

38. Early subacute hypoxic–ischemic encephalopathy (HIE) mimicking acute toxic
leukoencephalopathy in 15-year-old unresponsive boy after suicide attempt. CT findings were
negative (not shown). A and B, Severe extent of abnormality in periventricular white matter on
diffusion-weighted image(A) and apparent diffusion coefficient map (B) 6 days later. C, Bright
cortical and caudate signal on FLAIR (arrows) indicates HIE. Patient died 11 days after insult.

39. Renal Failure with Acute Toxic Leukoencephalopathy.

40. Reversible
leukoencep
halopathy
due to
carbon
monoxide
(CO).

41. leukoencephalopathy due
to due to drug toxicity.

42. Cerebellar
Hippocamp
al and Basal
Nuclei
Transient
Edema with
Restricted
diffusion
(CHANTER)
Syndrome.

43. 15 years old with Status epilepticus. Axial diffusion weighted images in a patient
with seizure disorder shows symmetrical diffusion restriction in bilateral
hippocampus. Complete resolution seen on follow up imaging (not shown).

44. Status epilepticus in a 2-year-old girl.
A, Coronal FLAIR image shows diffuse hyperintense lesions in the left hemisphere including
the left thalamus, cingulate gyrus, and hippocampus.
B and C, DW images show these lesions as hyperintense with decreased ADC. They
represent cytotoxic edema due to excitotoxic injury mediated by neuronal seizure activity.
These lesions were partially reversed on follow-up MR imaging (not shown).

45. Central pontine myelinolysis in a 14-year-old female adolescent. A, T2-weighted
image shows a hyperintense lesion in the pons. B and C, DW images show this
lesion a hyperintense with mildly decreased ADC. This finding represents
cytotoxic edema seen in the early phase of central pontine myelinolysis

46. Phenylketonuria in a 36-year-old man A, T2-weighted image shows hyperintense
lesions in the periventricular white matter. B and C, DW image shows these lesions
as hyperintense with decreased ADC. Excitotoxicity may be related to impairment
of glutamate receptor function by l-phenylalanine.

47. Glutaric aciduria in a 13-year-old male adolescent. A, T2-weighted image shows
hyperintense lesions in the bilateral globus pallidus (arrows) and diffusely in the
white matter. B and C, DW image shows these lesions as hyperintense with
decreased ADC. Excitotoxic injury may be due to an accumulation of organic
acids that share structural similarities with glutamate.

51. Maple syrup urine disease (a) Axial diffusion weighted images (DWI) image showing restricted
diffusion in bilateral middle cerebellar peduncles, (b) Axial DWI image showing restricted diffusion
in brainstem, (c) Axial DWI image showing restricted diffusion in corticospinal tracts.

52. Maple syrup urine disease Diffusion-weighted images with corresponding apparent diffusion
coefficient maps demonstrate restricted diffusion in the central part of the centrum semiovale (A, D);
posterior limbs of the internal capsules and thalami (B, E); and pons and cerebellar white matter (C, F)

53. Adrenoleukodystrophy and progressive vision loss in a 10- year-old boy. a Bilaterally
symmetric parieto-occipital signal changes are present (arrowheads) on the T2-W image.
b DW image shows low signal within the involved white matter (arrowheads). c ADC map
shows increased diffusion values within the regions of signal abnormality (arrowheads)

54. Canavan's disease with Diffusion restriction at the acute stage.

55. Canavan's disease. a-h Axial
MRIs. a DWI shows
hyperintensity in the internal
capsule and subcortical white
matter; B) ADC demonstrates
corresponding hypointensities; c
T2 FLAIR image; d T1 image. e
DWI with hyperintensities in the
subcortical white matter; f
Corresponding ADC
hypointensities; g T2 image;
d T1 image. Single voxel MRS
demonstrates increased NAA
(arrow, peak at 2.02 ppm;
choline, asterisk, 3.2 ppm;
creatine, arrowhead, 3 ppm);
inset shows area of analysis in
the posterior left hemisphere.

56. Canavan's disease in a 4-year child demonstrating typical diffusion restriction
of involving subcortical white matter and classical NAA peak on spectroscopy.

57. Acute Carbon Monoxide Poisoning.

58. Hypoglycemia induced restricted diffusion along bilateral posterior
limb of internal capsules and splenium of corpus callosum.

59. Early Diffusion
MR Imaging
Findings and
Short-Term
Outcome in
Comatose
Patients with
Hypoglycemia.

60. Reversible
hyperintensity
lesion on
diffusion-
weighted MRI
in hypoglycemic
coma.

61. Diffusion-
Weighted
Imaging of
Acute
Corticospinal
Tract Injury
Preceding
Wallerian
Degeneration
in the
Maturing
Human Brain.

62. A 16-year-old boy (patient 1)
presented with acute altered
mental status following
inhalation of heroin vapor.
Brain magnetic resonance
imaging demonstrates diffuse
symmetrical infratentorial (a–c)
and supratentorial (d–f) white
matter T2 hyperintensities. This
T2 prolongation shows
restricted diffusion with
increasing signal on diffusion-
weighted images (b) and (e)
with corresponding decreased
diffusion scalars on the
matching ADC map (c) and (f).
There is increased T2 signal of
the posterior paraspinal
muscles seen on axial (g) and
sagittal (h) images of the
cervical spine compatible with a
clinical diagnosis of
rhabdomyolysis affecting
predominantly the posterior
neck musculature

63. Complete
hemiplegia.
Following a
positive
urine
analysis, she
admitted
having taken
considerable
amounts of
cocaine.

64. Neonatal HIE in a 6-day-old boy with profound perinatal asphyxia.
A, On the T2-weighted image, gray matter–white matter delineation is partially
obliterated. The anterior and posterior aspects of the corpus callosum show high signal
intensity. B and C, DW images show diffuse hyperintensity with decreased ADC in the
corpus callosum (arrows), internal capsules, thalami, and white matter. This distribution
may be related to excitatory circuits. The neonatal brain seems to be highly vulnerable to
acute excitotoxic injury.

65. A 15 years old girl with HIE and resultant global diffusion restriction.

66. Neonatal HIE in a 10-day-old boy with profound perinatal asphyxia.
A, DW image shows extensive hyperintense lesions involving the frontotemporoparietal white matter,
internal capsules, and basal ganglia. B, DW image at the level of the midbrain shows hyperintense
lesions with decreased ADC (not shown) in the bilateral cerebral peduncles. These findings represent
the early phase of wallerian degeneration.

67. Shaken baby syndrome in a
2-year-old girl.
A, T2-weighted image shows
bilateral hyperintense lesions
in the frontal and temporo-
occipital lobes, basal
ganglia, and corpus
callosum. Subdural
hematomas are seen as
linear, hypointense lesions
along the interhemispheric
fissure (arrows).
B, T1-weighted image shows
subdural hematomas in the
posterior fossa in addition to
the interhemispheric fissure
(arrows).
C and D, DW images show
the brain parenchymal injury
as hyperintense with
decreased ADC that
represents cytotoxic edema
presumably due to injuries
with combined excitotoxic
mechanisms.

68. 8 years old with RTA Cerebral fat embolism with starry sky appearance.

71. Tumefactive
demyelinating plaque
in 41-year-old man.

72. 25-year-old woman with demyelinating lesion. A, Demyelinating plaque is seen in left middle
cerebellar peduncle (green circle) showing restricted diffusion with hypointense signal
intensity on apparent diffusion coefficient (ADC) map (A) and hyperintense signal intensity on
trace image (B). Notice no contrast enhancement is seen in that location on contrast-
enhanced T1-weighted image (C), reflecting hyperacute demyelinating plaque. On same
contrast-enhanced T1-weighted image, there is another focus of enhancement (blue circle,
C), located in right cerebellar peduncle close to fourth ventricle wall, with hyperintense signal
on trace image (blue circle, B) and isointense signal on ADC map (blue circle, A), representing
most common demyelinating lesion behavior on diffusion-weighted imaging.

74. 37-year-old man with spinal cord demyelinating lesions.

76. 8-year child with ADEM demonstrating peripheral rim like
diffusion restriction and incomplete ring enhancement.

80. Fourth ventricle medulloblastoma in 4year
child demonstrating diffusion restriction.

86. GBM. Left parieto-occipital lesion with peripheral vasogenic edema. DWI and ADC (a and
b, respectively) show a clear area of increased diffusion within the core, corresponding
to a necrotic centre. On T1 3D post gadolinium the mass shows ring enhancement

89. Primary CNS
lymphoma. Left
frontal periventricular
lesion showing
prominent diffusion
restriction, presenting
with hyperintensity
on DWI (a), low ADC
value (b) and mild
hyperintensity on
T2WI (c), all typical
features of this type
of hypercellular
tumour. T1WI post
gadolinium (d) shows
homogeneous and
intense contrast
enhancement.

92. Meningothelial meningioma
in the left high frontal
convexity.
A, On a T2-weighted image,
tumor is mildly high in
intensity.
B, Tumor enhances
homogeneously on a T2-
weighted image.
C, The tumor is of high
intensity on DWI.
D, Regions of interest are
shown on the ADC map. The
ADC values are 0.76, 0.63,
and 0.55, and the averaged
ADC value is 0.65. Restricted
diffusion in the tumor
probably is caused by high
tumor cellularity.

93. Fibrous meningioma in the left
convexity. A, On a T2-weighted
image, tumor intensity is mildly
high and edema is present anterior
to the tumor.
B, The tumor enhances
homogeneously.
C, On DWI, the peripheral portion
of the tumor is moderately
hyperintense and the central
portion is isointense. Peritumoral
edema is mildly high in intensity.
D, Regions of interest are shown on
the ADC map. The ADC values are
0.83, 0.74, 0.71, 0.67, and 0.57,
and the averaged ADC value is
0.70. Some areas of apparent
restricted diffusion in the tumor
probably reflect T2 shine-through
effect, because ADC values in these
areas are not low and the signals
in those areas show high intensity
on the T2-weighted image.

102. Abscess. Right occipital mass showing marked diffusion restriction within the core on
DWI and ADC maps (a and b, respectively) and a peripheral enhancing pattern on T1
post gadolinium (c). DWI helps to differentiate ring-enhancing lesions because restricted
diffusion in the centre of the mass is characteristic of pyogenic abscesses. In this case,
diffusion-based sequences also helped to identify ventriculitis (arrows).

109. Subacute hematoma. Right parietal mass (arrowhead) showing diffusion restriction within the core
on DWI and ADC maps (a and b, respectively) and a ring-enhancing pattern on T1 post gadolinium (c).
This was a subacute hematoma. Clinical context is important to differentiate hemorrhage from
abscess. There is also a subacute ischaemic lesion in the inferior right frontal lobe (arrows) that shows
early pseudonormalisation of the ADC and gyriform enhancement post gadolinium

110. Optic neuritis. High
DWI signal (a) and
low ADC value (b)
representing
restricted diffusion
in the right optic
nerve in a patient
with non-specific
optic neuritis.

112. A 10 year boy with status post operative for glioblastoma and now
demonstrates linear diffusion restriction along the ependymal
surface of right lateral ventricle and also along the septum.

113. Post-surgical ischemia.
Immediate follow-up MRI in
a patient who underwent
surgery for resection of a
suspicious enhancing mass.
In the medial aspect of the
resection cavity (asterisk)
there is an enhancing area
on the T1 post-contrast
sequence (c, arrow). This
finding alone could
represent residual tumour,
but the presence of
restricted diffusion with
high signal on DWI (a) and a
low ADC value (b) meant
that a small area of peri-
surgical ischemia was more
likely. Three-month follow-
up T1 post-gadolinium MRI
(d) shows absence of
enhancement in the same
region (arrowhead),
confirming this diagnosis.

114. Conclusion.
Diffusion-weighted sequences currently play a central
role in neuroimaging. The already widespread qualitative
assessment allowed by these sequences improves
sensitivity in the depiction of several central nervous
system conditions, whereas new models of diffusion
sequences provide quantitative parameters, allowing
potential biomarkers for diagnosis, prognosis and
follow-up. The future of DWI will undoubtedly include
technical improvements to enhance data fidelity, to
achieve high isotropic resolution (e.g., submillimeter)
for 3D acquisitions and to reduce the image acquisition
time. Furthermore, advances in ultrahigh field
technology are already being applied to DWI.

115. Thank You.