Transcript Physics and its applications in non-stroke brain

THE DWI-ADC
Physics and its applications in non-stroke brain pathologies
Sangam Kanekar, MD
Dept of Radiology
Milton S Hershey Medical Center
INTRODUCTION
Introduction: Diffusion-weighted (DW) MR imaging has enabled us in evaluating
structural and physiological states in biologic tissue by measuring the microscopic
motion of the water proton. Due to its ability to diagnose cytotoxic edema it has become
the main armour in the imaging of stroke, which in corelation with ADC can be
diagnosed within 30 mts. Over the period of time it has been find out that there are
various other pathologies which can show restricted diffusion and thus bright on DWI,
due to various reasons. In this exhibit we discuss the basic physical principle behind the
DWI sequence and discuss the various diffusion positive non-stroke lesion of the brain.
PHYSICS
Fundamentals of DWI is based on the Brownian movement of water in tissues. What is
Brownian movement ? Every molecules in any living tissue routinely undergo random
(brownian) motion.
Tissues with unrestricted water diffusion, the MR signal is dispersed and attenuated and
thus appear low intensity on DWI. If there is restriction of water diffusion due to some
reasons there is increases the signal intensity on DWI.
DWI in Arachnoid cyst
DWI in Abscess
PHYSICS
Information regarding the brownian motion is obtained by DWI sequence. Isotropic
DW is typically obtained by measuring loss of signal after a pulse sequence that
consists of a series of two sequential gradient pulses added to a 90°–180° spin-echo
sequence on either side of the 180° pulse.
The degree signal loss after application of the second gradient pulse is related
to two factors:
(a) the duration and strength of the magnetic field gradients (b)
(b) the diffusion coefficient of the substance (D).
The degree of signal loss is represented by S/So.
S= signal after application of diffusion gradients AND
So= signal before use of diffusion gradients
Signal attenuation is described by the formula:
S/S0 = exp (- b-factor x ADC)
S/S0
Ratio of Signal with diffusion gradients to Signal without diffusion gradients
b-factor Attenuation factor [s/mm2], diffusion gradient dependent.
ADC
Apparent Diffusion Coefficient [μ m2/s], tissue dependent.
PHYSICS
DWI SEQUENCE
Single short diffusion sequence
180 *
90 *
diff Gr
diff Gr
TE
Multi short diffusion sequence
180 *
90 *
diff Gr
diff Gr
diff TE
actual TE
TE
PHYSICS
ADC
Signal attenuation in diffusion weighted imaging depends on the strength and timing of the
diffusion gradients. The amount of signal attenuation is controlled by the b-factor. However,
movability of the spins in biological tissue is limited by the tissue itself, and also by cell walls.
Signal decay also depends on the extent of the physiological compartments .
What is ADC?
The observed signal decay can be used to calculate the diffusion properties, or the Apparent
Diffusion Coefficient (ADC). Mobile molecules experience a substantial loss of signal that is
related to the diffusion coefficient and spin-spin relaxation time (T2) of tissue, as well as the
pulse sequence parameters chosen by the operator (eg, b value and excitation time). ADC is a
value that describes microscopic water diffusibility in the presence of factors that restrict
diffusion within tissues.
In tissues, DWI probes the movement of water molecules, which occurs largely in the
extracellular space. However, the movement of water molecules in the extracellular space is not
entirely free, but is modified by interactions with hydrophobic cellular membranes and
macromolecules. Hence, diffusion in biological tissue is often referred to as "apparent diffusion".
By comparing differences in the apparent diffusion between tissues, tissue characterization
becomes possible. For example, a tumour would exhibit more restricted apparent diffusion
compared with a cyst because intact cellular membranes in a tumor would hinder the free
m o v e m e n t
o f
w a t e r
m o l e c u l e s .
Tumors & DWI-ADC
The rationale of adding DWI in the tumor evaluation is to quantify cellularity. Water
diffusivity within the extracellular compartment is inversely related to the content and
attenuation of the constituents of the intracellular space. Various studies have found an
inverse correlation between the ADC and tumor cellularity. Higher the tumor cellularity,
lower is the apparent diffusion coefficient (ADC). Decrease in the water diffusivity is
due to relative reduction in extracellular space by the compact neoplastic cells. ADC
values have also been shown to have inverse relation with the choline peak at MR
s p e c t r o s c o p y a n d i s p o s i t i v e l y c o r r e l a t e d w i t h t u m o r c e l l d e n s i t y.
Note: The role of ADC in grading the cellularity of glioma appears less promising
because of the limitation of ADC as a quantitative biomarker of cellularity and because
of inherent and quite remarkable tissue heterogeneity associated with gliomas across
different grades, within the same grade, and even within a single given tumor.
NEOPLASM
INTRODUCTION: The grade of brain tumor is desicive factor in the treatment and
prognosis. Though routine MR sequmces are very sensitive in diagnoses of neoplasm,
grading of cellularity and identifying the perilesional presence of tumor cells have been
a challenge. DWI-ADC to some extent along with perfusion may be helpful in assessing
the tumor grade and cellularity, postoperative injury, peritumoral edema, and integrity of
w
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a
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t
s
Based on tumor cellularity, nuclear atypia, mitotic activity, pleomorphism, vascular
hyperplasia, andnecrosis gliomas have been classified into 4 grades (I–IV), where I is
relatively benign (eg pilocytic astrocytoma, PXA, SGCA) while IV is highly malignant
and has worse prognosis.
NEOPLASM
Neoplasm
Water diffusion has been found to be restricted in cellular brain tumors such as
medulloblastoma, primitive neuroectodermal tumors. Restricted diffusion is believed to
be due to increased cellularity, decreased extracellular space, and high nuclear-tocytoplasmic ratio in high-grade tumors. Further in animal models it has been
demonstrated that ADC increases during chemotherapy when there is a reduction in
cellularity and more extracellular space and decreases back to baseline with tumor
recurrence.
DWI
ADC
+Gd
Medulloblastoma restricted on DWI
NEOPLASM
DWI and GLIOMAS
Introduction: It is known that high grade gliomas often contains a continuum of histologic
features and thus ADC values within such tumor will vary markedly, underscoring the the
spectrum of glioma cellularity. It should also be well understood that tumor grade will entirely
depend on the site of tumor biopsy or resection, subjecting it to sampling error. The signal
intensity of gliomas on DW images is variable and a subtle hyperintensity is a commonly seen
nonspecific finding. ADC values are usually in the range of 0.82 to 1.14 (x 10-3 mm2/sec). As
said in the introduction ADC values cannot be used to differentiate and grade gliomas. Also
DWI-ADC maps cannot distinguish neoplastic infiltration from peritumoral edema.
ADC
+Gd
DWI
NEOPLASM
DWI and GLIOMAS
DW Imaging for Grading Tumors: Multiple studies have shown lower water diffusibility in
high-grade gliomas than in lower grade gliomas. However there is considerable overlap between
ADCs in high and low grade tumors making it difficult to use ADC as a biomarker to measure
cellularity and hence grading. It remains doubtful whether tumor grade can be evaluated with
enough specificity with DW imaging to be useful in a clinical context. At present DWI-ADC
cannot be used to differentiate between high and low-grade gliomas or between tumor types.
ADC
DWI
DWI
Oligodendroglioma
No restricted diffusion on DWI
GBM
No restricted diffusion on DWI
NEOPLASM
DWI and definition of Tumor Margins: A number of studies have shown that ADCs in
peritumoral edema are higher for metastases than for primary cerebral tumors. To date, any role
for DW or diffusion-tensor imaging in the evaluation of vasogenic edema surrounding a mass
remains speculative. Studies have showed considerable overlap between the ADCs of tumor and
peritumoral tissues thus found that addition of DW imaging to a conventional tumor imaging
protocol provided no important additional diagnostic information.
+Gd
ADC
GBM: infiltrative tumor with extensive vasogenic
edema, shows variable ADC values.
NEOPLASM
Vasogenic v/s Infiltrative edema in GBM
DWI imaging can be used to reliably distinguish vasogenic from cytotoxic edema. Whereas
cytotoxic edema is characterized by restricted diffusion while vasogenic edema will show
elevated diffusion. On DW MR images, vasogenic edema is hypointense to slightly hyperintense,
due to T 2 shine through. Differentiation between vasogenic and infiltrative edema has been
attempted with DWI, on the basis that infiltrative edema will have lesser diffusibility as
compared to the vasogenic edema due to compact malignant cells. But this rule, due to
heterogenity of the tumor pathology, does not hold true. Several reports have shown that ADC
values are not helpful in differentiating tumor and tumor related brain edema.
DWI
ADC
+Gd
DWI with extensive cytoxic-infiltrative edema from GBM
NEOPLASM
DWI & POST-OPERATIVE CHANGES
Restricted diffusion abnormality is not always diagnostic of acute cytotoxic edema, it can be seen
in numerous intracranial diseases. Any process that results in acute intracellular swelling and
subsequent decrease in the surrounding extracellular space can lead to reduced proton diffusion in
the brain.
Following tumor resection, acute cellular damage may be due to variety of reasons such as direct
surgical trauma, retraction and vascular injury, and devascularization of tumor. Restricted
diffusion in and around the site of surgery is not uncommon. Regions of reduced diffusion with
contrast enhancement on a follow-up study may not always be dianostic of recurrent tumor. On
long term follow-up these area has been shown to be either encephalomalacia or gliotic cavity.
T2
T1
DWI
Status post tumor resection DWI changes
NEOPLASM
LYMPHOMA
Lymphomas show iso to hypointense signal relative to gray matter on T2-weighted
images and enhance homogeneously. Rim enhancement may be seen in
immunocompromised patients. High signal intensity on DW images and low ADC
values may favor the diagnosis of lymphoma versus glioma or metastasis. Lower ADC
is likely due to higher cellularity.
FLAIR
+Gd
DWI
DWI restricted in lymphoma
NEOPLASM
LYMPHOMA
DWI
ADC
DWI
+Gd
ADC
DWI is commonly used in diagnosis and to differentiate other tumors from lymphoma. Bright
signal on DWI is proven to be due to high cellularity and corresponding decrease in the
extracellular fluid and thus restriction of the fluid. ADC have been found to be decreased in
lymphomas relative to other intracranial tumors such as high-grade gliomas, metastases, or
meningiomas.
NEOPLASM
EPENDYMOMA
Ependymomas arise within IV ventricle and extend through its outlets, They are well
differentiated, moderately cellular gliomas with perivascular pseudorosettes (cleared areas and
radially arranged cells around blood vessels), rare mitoses with ocasional areas of necrosis,
hemorrhage and calcification. The typical cellularity of ependymomas is somewhere between that
of astrocytomas and medulloblastoma. Some of them may be very cellular. ADC values for
ependymoma are usually between 1.05–1.33 as compared to medulloblastoma 0.58-0.99.
+Gd
ADC
DWI
NEOPLASM
MENINGIOMA
Meningioma are easily diagnosed by cross sectional modality. But till today differentiating and
grading the various types is difficult. It was thought that atypical (WHO grade 2) and anaplastic
(WHO grade 3) meningiomas exhibited lower ADC than that of benign meningioma. However,
as per Kono et al study, the ADC is not indicative of the histologic subtype of meningiomas. Our
study also had similar observation in few meningiomas.
+Gd
DWI
ADC
Restricted diffusion in highly cellular left frontal
meningioma.
NEOPLASM
MENINGIOMA
+Gd
DWI
ADC
Like other benign tumors, signal intensity of meningiomas on DWI is variable. Most benign
meningiomas are isointense on DW images and ADC maps. High signal intensity on DW images
and reduced ADC values suggest malignant meningioma and is again though to be due to high
cellularity and corresponding decrease diffusion.
NEOPLASM
METASTASIS
Majority of the metastasis are iso to low signal on DWI and are high on ADC. But the signal
intensity of these lesions may change depending on the histiology and composition (ie, solid
tumor, degeneration, hemorrhage, and cyst). In addition SI on DWI is influenced by T2, the ADC,
b value, spin attenuation, and TE used. Small cell carcinoma, adenocarcinoma may commonly
show bright signal on DWI and reduced ADC. Studies have concluded that their appearance on
MR imaging most likely reflected the inherent T2 effect of the tissue (the blood products calcium,
mucin, and iron).
DWI
ADC
+Gd
DWI+ Metastasis from adenocarcinoma of the
lung
NEOPLASM
METASTASIS
In metastatic brain tumors or noninfiltrative primary tumors such as meningiomas, the
peritumoral edema is synonymous with vasogenic edema, where there is increased extracellular
water due to leakage of plasma fluid from altered tumor capillaries but no tumor cells are present.
In gliomas, however, the peritumoral edema is better referred to as infiltrative edema, because it
represents both vasogenic edema and infiltrating tumor cells that are behind the BBB and usually
invading along the white matter tracts.
+Gd
ADC
DWI
COLON CANCER METASTASIS
NEOPLASM
EPIDERMOID
Epidermoid tumors are benign developmental tumors, with debris, keratin, water, and cholesterol.
On T1 WI these tumors are mildly hypointense, while on FLAIR they show mild hyperintensity.
On T2WI they are very difficult to differentiate from arachnoid cyst.
T2
T2
V/S
DWI
Fig. CP angle Epidermoid: Axial T2 & T1WI
show a cystic mass in the left cerebellopontine angle
causing anterior bowing of the VII-VIII nerve
complex. This cyst is restricted on DWI which is
very classical for epidemoid cyst.
DWI
Fig: Arachnoid Cyst: Cystic intensity mass lesion is
seen in the right CP angle cistern compressing &
displacing the VII-VIII nerve complex anteriorly.
NEOPLASM
DWI
Case 1
DWI
ADC
Case 2
DWI+ Intraosseous epidermoid
DWI+ petrous apex epidermoid
EPIDERMOID CYST/ ECTODERMAL INCLUSION CYST: 90% are intra-dural in the basal
cistern. 40-50% of these lesions are in CPA and 17% in fourth ventricle. They are lobulated,
irregular, cauliflower like mass with fronds that insinuate into cistern, and encases nerves &
vessels. On CT, 95% of the time they show CSF density and fail to show any enhancement.
Epidermoid cysts show restricted diffusion on DWI. Arachnoid cysts demonstrate free diffusion
of water similar to that of CSF, whereas epidermoids show slower diffusion, presumably as a
result of the more complex internal structure.
INFECTION
INTRODUCTION:
Ring enhancing lesion, whether solitary or multifocal is always a clinical and radiological
dilemma. The differential diagnosis of intracerebral necrotic tumors and cerebral abscesses is
frequently impossible on conventional MR images. With DWI being routinely incorporated in the
imaging of brain, differential diagnosis can be either narrowed or yet times specific diagnosis
may be given.
Restriction on DWI with low ADC values is seen within the pyogenic abscess cavity. Low ADC
values (0.28 and 0.70 103 mm2/s) is ascribed to the presence of intact inflammatory cells and
bacteria which impede the microscopic motion of water molecules. Following surgical drainage
of pus or on medications ADC shows high signal and has been shown to correlate with good
therapeutic response.
+Gd
DWI
ADC
Fig: Frontal lobe abscess due to frontal sinusitis with erosion and break in the frontal
bone.
INFECTION
ABSCESS
T2
+Gd
DWI
Fig: Multiple ring enhancing lesions: Differential
diagnosis include abscesses, metastasis, granulomas.
+Gd
Multiple ring enhancing lesions are always
difficult to typify as the clinical findings may
Fig: Single parietal lobe abscess: Pt presented with history
be overlapping. Although highly sensitive, CT of seizure.
scanning is not specific.
Even on routine conventional MR besides abscess, similar findings may also be seen in cerebral
neoplasms, cerebrovascular accidents or granulomas. However, DWI may help in giving a
specific diagnosis due to central area of restricted diffusion and low ADC.
The ADC values of abscess fluid are markedly lower than those of necrotic or cystic portions of
tumor, which is considered to be a consequence of restricted water mobility within purulent fluid
related to its high cellularity and viscosity.
INFECTION
ABSCESS
+Gd
Pretreatment
DWI
Fig: Pre and post treatment multiple brain abscesses shows
change in the DWI-ADC signal following treatment.
It is well documented that the treated abscess
shows corresponding changes in the DWI-ADC
changes. As the abscess responds to the antibiotic
or therapy, restriction within the abscess
decreases and ADC value increases. This
definitely helps in confirming the respons to the
a d m i n i s t e r e d
t h e r a p y .
DWI
Postreatment
ADC
INFECTION
ABSCESS
+Gd
DWI
ADC
DWI
Fig: Histologically proven left maxillary abscess shows
restricted diffusion with corresponding low ADC.
Fig: Bilateral parotid abscesses with diffuse
parotid and neck lymphadenopathy in
immunocompromised patient.
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 fibrinogen, also may play a key
role in restricting the diffusion of protons in pus.
INFECTION
VENTRICULITIS
Ebisu et al (Magn Reson Imaging 1996; 14:1113-1116 ) performed in vitro DW imaging and ADC
measurement of aspirated pus. The pus imaged in vitro showed high signal intensity and low
ADC values, similar to the results of the in vivo study. Thus, they concluded that the pus
structure itself is responsible for the signal changes on DWI and low ADC values. DWI changes
were due to heavily impeded water mobility of pus which were in turn related to its high
cellularity and viscosity.
DWI
DWI
Subdural empyema and ventriculitis shows restricted
diffusion
INFECTION
SUBDURAL EMPYEMA
+Gd
DWI
ADC
Subdural empyema following frontal sinusitis with DWIADC changes
SDE is most commonly seen in infants following purulent meningitis, while in older children, it
is due to direct extension of sinusitis or otitis media into the extracranial spaces. Reactive
subdural effusion (RSE), which is also seen in meningitis, is due to tears in the arachnoid
membrane leading to CSF leakage in the subdural space. Differentiating SDE and RSE is critical,
as RSE tends to spontaneously regress, whereas SDE generally requires aggressive intervention.
Differentiation is difficult using conventional MR sequences since both are hyperintense on
T2WI, and both may show peripheral enhancement on +C T1WIs. DWI is very helpful in
diagnosis of SDE, since it shows restricted diffusion in empyema and not in RSE.
INFECTION
TB & FUNGAL INFECTION
+Gd
DWI
ADC
Low ADC has also been observed in tubercular and fungal abscesses, and is considered to be the
result of the presence of proteinaceous fluid and cellular infiltration in the pus. It may not be
always possible to differentiate these two. Fungal cerebral abscesses show decreased diffusion,
similar to pyogenic abscesses and therefore should be included in the differential diagnosis of
ring-enhancing lesions with centrally restricted diffusion, especially in immunocompromised
patients. Few studies also proposed that the DWI showed restricted diffusion in the projections
and wall of the fungal abscess and not in the center, whereas the pyogenic and tubercular group
showed restricted diffusion in the core of the cavity.
INFECTION
HERPES ENCEPHALITIS
T2
DWI
DWI
Fig Bilateral herpes encephalitis. T2WI show left temporal hyperintensity while DWI for the same patients shows restricted diffusion
bilaterally suggesting bilateral herpes encephalitis.
Herpes encephalitis lesions may show restricted diffusion with ADC values similar to the normal
brain parenchyma, which on follow up scans these areas may demonstrate encephalomalacic
change. The restricted diffusion is thought to be due to cytotoxic edema in tissue undergoing
necrosis. DWI may be useful in differentiating encephalitis from infiltrative tumors. ADC values
are low in herpes while tumor usually shows elevated or normal ADC range.
INFECTION
a
b
c,d
Fig. West Nile Encephalitis: (a) Axial CT at level of basal ganglia shows hyperdensity in thalami and caudate
heads from petechial hemorrhages. (b-d) Axial MR images. (b)T1W image shows symmetric hyperintense signal in
DGMN due to tiny hemmorhages. (c,d) DWI shows abnormal bright signal intensity in DGMN and cerebral white
matter.
While West Nile Encephalitis (WNE) is endemic in the Middle East, Africa and Asia, in the US,
WNE is mainly seen in Northeast states. It is an arthropod-borne (mosquito) disease manifesting
as encephalitis. Specific diagnosis requires serum testing with enzyme immunoassay and the
plaque reduction neutralization test. MR often helps to exclude other infectious conditions,
including herpes encephalitis. In the early stages of WNE, MRI may be normal. Later,
involvement of the brain stem, substantia nigra and anterior horn of the spinal cord are identified.
Petechial hemorrhages and DGMN involvement are also seen in later stages. DWI may show
bright signal intensity either due to T2 shine through or cytotoxic damage.
INFECTION
CREUTZFELDT JACOB DISEASE
DWI
ADC
sporadic CJD
variant CJD
CREUTZFELDT JACOB DISEASE (CJD) is a very uncommon cause of dementia and is frequently
accompanied by myoclonus. There are thought to be four forms of CJD: sporadic, iatrogenic,
familial and variant. Overall, the majority of cases of human prion disease are sporadic. The peak
onset between 45 to 75 yrs. Pathology: is characterized by spongiform change, neuron loss and
astrocytosis. In sporadic CJD, MR is quite characteristic & shows bilateral, but either
asymmetric or symmetric, increased signal on T2 weighted images in the caudate and putamen.
In the variant CJD the most characteristic abnormality is reported to be high intensity on T2
weighted images in the pulvinar of the thalami, termed as “ pulvinar sign”.. ADC may be
significantly lower or normal or mildly elevated. This variability is related to variable amounts of
spongiform change, neuronal loss, and gliosis. These changes does help in differentiating CJD
from other dementias. In addition conventional MR may be normal in as many as 21% of CJD.
INFECTION
PROGRESSIVE MULTIFOCAL LEUKOENCEPHALOPATHY (PML)
PML is a CNS infection of the immunocompromised caused by the group B human papoviruses,
typically the Jacob-Creutzfeldt (JC) and Simian Virus (SV) 40 viruses. Their target is the
oligodendrocyte—the cell responsible for the production of myelin. Impaired replenishment of
myelin rather than “destruction” of existing myelin and this explains the long time interval
between the initial HIV infection and the appearance of this disease. The attack on the
oligodendrocytes tends to be patchy and progressive which is why the white matter is affected.
DWI
T2
FLAIR
+CT1
Fig. Progressive multifocal leukoencephalopathy. T2 & FLAIR images at the level of the lateral ventricles reveal a
subcortical, hyperintense signal abnormality in the right hemisphere. The lesion appears restricted to the white matter
and does not exhibit mass effect. The lesion did not enhance with contrast administration. The appearance is most
consistent with progressive multifocal leukoencephalopathy.
DEMYELINATING DISEASES
MULTIPLE SCLEROSIS
DWI
DWI
The signal intensity of multiple sclerosis (MS) on DW images is variable. Most plaques
demonstrate increased diffusion. Acute plaques have significantly higher ADCs than do chronic
plaques due to increase in the size of the extracellular space due to edema and demyelination
acutely and to axonal loss and gliosis chronically. ADC values have shown to be (1.35 x 10-3
mm2/sec) significantly higher than those for normal-appearing white matter (mean, 0.77 x 10-3
mm2/sec).
DEMYELINATING DISEASES
MULTIPLE SCLEROSIS
DWI
ADC
+Gd
Restricted diffusion seen on the DWI in acute
demyelinating plaques of MS
Occasionally, MS lesions may show restricted diffusion with
low ADC values and is thought to be due to shifts in
intracellular water protons and changes in membrane
permeability. The influx of inflammatory cells and
associated macromolecules may also lead to restriction of
water diffusion and reduction in trace ADC. Studies have
also shown an increase in ADC values in normal-appearing
w h i t e
m a t t e r
o f
M S .
DWI
DEMYELINATING DISEASES
ACUTE DISSEMINATED ENCEPHALOMYELITIS
DWI
ADC
+Gd
Fig. ADEM Axial FLAIR & DWI-ADC images show abnormal hyperintensity in
the temporal and frontal lobes at gray- white matter junction. Lesion in the left globus
pallidus and splenium shows restricted diffusion.
MR is highly sensitive and shows demyelinating lesions scattered in the cerebral and cerebellar
white matter without mass effect. Posterior fossa involvement is more common in children. These
lesions show high ADC, likely as a result of demyelination and increased extracellular water.
Rarely some areas may show restricted diffusion. DWMR imaging cannot help distinguish
between MS & ADEM, but can certainly differentiate these two conditions from stroke.
HEMORRHAGE
Note: The appearance of hemorrhage on DW MR images is complex and depends on multiple
factors, like different hemorrhagic products and the pulse sequence used.
Restricted changes noted on DWI in early stages of intracranial hemorrhage are multifactorial: 1)
A shrinkage of the extracellular space with clot retraction, 2) A change in the osmotic
environment once blood becomes extravascular, which alters the shape of RBC, 3) the formation
of the fibrin network associated with clot, 4) A conformational change of the hemoglobin
macromolecule within the red blood cell.
STAGE
T1WI
T2WI
DWI
ADC
Hyperacute / Intracellular oxyHb
Iso/ hypo
Hyper
Hyper
Low
Acute/ Intracellular deoxyHb
Iso/ hypo
Hypo
Hypo
Cannot be
calculated
Early acute/ Intracellular methmoHb
Hyper
Hypo
Hypo
Cannot be
calculated
Late subacute/ Extracellular methmoHb
Hyper
Hyper
Hyper
Hyper
HEMORRHAGE
DWI
OxyHb is hyperintense on DW images and has a lower ADC than does normal brain
tissue; this may indicate the relative restriction of water movement inside the red blood
cell. Hyperacute clot are markedly hyperintense on DWI, acute clots are markedly
hypointense, early subacute clots are hypo & late subacute clots are hyperintense.
HEMORRHAGE
Acute/ Intracellular deoxyHb
Early acute / Intracellular MethHb
It has been demonstrated that the diffusion is reduced in hyperacute, acute, and subacute clots.
Reduced ADC accounts for the marked hyperintensity on DWI scans in hyperacute and late
subacute phases. Despite restricted diffusion, SI on DWI is not increased in the intervening acute
and early subacute phases because of T2-induced hypointensity of clot, which dominates signal
intensity on DWI (“T2 dark-through). Hemorrhage containing deoxyhemoglobin, intracellular
methemoglobin, and hemosiderin are hypointense on DW images because of magnetic
susceptibility effects. Because these products of hemorrhage have very low signal intensity on
T2-weighted images, ADCs cannot be reliably calculated for them.
INJURY/INSULT
DIFFUSE AXONAL INJURY
INTRO: Diffuse axonal injury results from shearing forces at the interface between brain
structures with different density and rigidity. Extensive tissue at multiple sites may lead to
profound neurologic deficits especially when trauma is coupled with hypoxia and hypotension.
Though the exact mechanisms underlying the changes in diffusion associated with diffuse axonal
injury are not yet fully understood, experimentally (rat study) it has been proposed that bright
areas on DWI are not due to ischemic edema but rather due to neurotoxic edema causing the
r e d u c e d
A D C s
a n d
n e u r o n a l
i n j u r y .
ADC
DWI
DWI
ADC
INJURY/INSULT
DIFFUSE AXONAL INJURY
Schaffer et al found that among all of the sequences investigated, diffusion-weighted sequences
showed the strongest correlation between lesion volume and subacute modified Rankin score at
discharge. Diffusion-weighted imaging can demonstrate lesions that are not visualized with
conventional MR sequences. Radiology October 2004 Volume 233 Number 1 Schaefer et
Study also proposed that (a) the majority of diffuse axonal injuries identified were characterized
by changes in water diffusivity; (b) DWI demonstrates increased contrast-to-noise ratio,
compared with conventional sequences; and (c) DWI is vulnerable to susceptibility effects and,
t h e r e f o r e , d e p i c t s m a n y h e m o r r h a g i c l e s i o n s .
GRE
ADC
DWI
INJURY/INSULT
PRESS
The cause of PRES is controversial. IT may be seen with eclampsia, cyclosporine/ FK-506
toxicity & systemic chemotherapy. If diagnosed early and treated patient will have no to little
residual defect. However unrecognized condition can progress to ischemia, massive infarction,
and even death. DWI is very reliable in distinguishing vasogenic from cytotoxic edema in the
setting of cerebral ischemia. It has been hypothesized (Diego J. et al AJNR Am J Neuroradiol 23:1038–1048, June/July 2002).
that 1) that the extent of regional involvement by vasogenic edema in PRES has prognostic
implications and can help in identifying patients who need more aggressive treatment, 2) that
severe vasogenic edema can progress to cytotoxic edema, and 3) that DWI can help in predicting
the conversion to infarction and irreversible tissue damage.
ADC
DWI
INJURY/INSULT
ETHYLENE GLYCOL TOXICITY
DWI
ADC
DWI
ADC
Ethylene glycol is metabolized in the liver, and ultimately, glyoxylic acid is converted
to oxalic acid, which precipitates in the presence of calcium as calcium oxalate crystals.
This pathway is responsible for the metabolic acidosis and toxic symptoms. Restricted
diffusion is most probably due to cytotoxic edema and presence is indicative of poor
outcome.
INJURY/INSULT
PROFOUND HYPOXIC DAMAGE
DWI
ADC
DWI
Mostly seen after prolonged or acute profound hypoxic injury. Cardiac
arrest in adult while nuchal cord/uterine rupture are the commonest
causes in adult & infant respectively. The outcome in this patient is
decided by the duration of insult to the affected brain. In profound cases
there is no time for the “diving reflex”(redistribution of blood from cortex to
deep gray nuclei) and therefore both the cortex as well as the deep gray
matter nuclei are involved. It classically involves the posterior part of
the putamen, lateral thalami and Rolandic cortex.
INJURY/INSULT
ACUTE WERNICKE’S ENCEPHALOPATHY
ADC
DWI
DWI
Without thiamine, the Krebs and pentose phosphate cycles cannot
metabolize glucose leading to cellular failure, and midline gray matter
degeneration leading to WE. Pathologic changes include necrotic lesions in
the mamillary bodies, periaqueductal gray matter, and walls of the III & IV
ventricle.
Microscopic exam shows pleomorphic microglia, decreased myelination, edema, swollen
astrocytes, prominent blood vessels in these regions. MR findings are in parallel with pathologic
changes: T2 & FLAIR show bright signal in the above regions. DWI is very rarely positive with
corresponding ADC changes possibly due to microscopic changes associated with it.
METHOTREXATE TOXICITY
DWI
ADC
The pathophysiology of methotrexate neurotoxicity is unclear. Several mechanisms
have been proposed. These include increased adenosine accumulation, homocysteine
elevation and its excitatory effects on the N-methyl-D-aspartate (NMDA) receptor, and
alterations of biopterin metabolism. The MR imaging findings of increased signal
intensity on DWI with hypointensity on apparent diffusion coefficient (ADC) map are
indicative of cytotoxic edema. This is consistent with the proposed mechanisms of a
direct neurotoxic effect of methotrexate on the cell.
Conclusion
 Besides stroke, DWI-ADC can be sensitive and specific
for various CNS pathologies.
 DWI-ADC provides the viability information of the
brain tissue.
References
1. Diffusion-weighted MR Imaging of the Brain Radiology 2000; 217: 331. Pamela W.
Schaefer, P. Ellen Grant, and R. Gilberto Gonzalez
2. Diffusion MRI: precision, accuracy and flow effects. NMR Biomed 1995; 8:307-332
Conturo TE, McKinstry RC, Aronovitz JA, Neil JJ.
3. MR imaging of high-grade cerebral gliomas: value of diffusion-weighted echoplanar
pulse sequences. AJR Am J Roentgenol 1994; 162:671- 677 Tien R, Felsberg G, Friedman H,
Brown M, MacFall J
4. Diffusion and perfusion magnetic resonance imaging: applications to functional MRI
New York, NY: Raven, 1995. Le Bihan D
5. Basic principles of diffusion-weighted imaging European Journal of Radiology 45 (2003)
169-184 Roland Bammer
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