Original Paper
Received: October 15, 2001
Cerebrovasc Dis 2002;14:187–196
DOI: 10.1159/000065675
Diffusion-Weighted Imaging in Acute
Stroke – A Tool of Uncertain Value?
Jens Fiehler a Jochen B. Fiebach b Achim Gass c Mathias Hoehn i
Thomas Kucinski a Tobias Neumann-Haefelin d Peter D. Schellinger e
Mario Siebler f Arno Villringer g Joachim Röther h
for the ‘Kompetenz Netzwerk Schlaganfall’
Departments of Neuroradiology, University Hospitals of a Hamburg-Eppendorf, Hamburg and b Heidelberg,
Departments of Neurology, University Hospitals of c Heidelberg-Mannheim, d Frankfurt, e Heidelberg, f Düsseldorf,
g Charité, Berlin and h Hamburg-Eppendorf, Hamburg, and i Max Planck Institute for Experimental Neurology,
Cologne, Germany
Key Words
Stroke W Magnetic resonance imaging W Diffusion
Abstract
The concept of a mismatch between the lesion volume in
diffusion- and perfusion-weighted magnetic resonance
imaging (MRI) indicating ‘tissue at risk of infarction’ is
based on the assumption that tissue with diffusion slow-
ing in diffusion-weighted MRI (DWI) or decreased values
of the apparent diffusion coefficient represents irrevers-
ibly damaged tissue. Recent experimental as well as clin-
ical studies, however, have shown that tissue with diffu-
sion slowing may well normalize if the hypoperfusion is
moderate or transient. We will interpret these findings in
the light of experimental data and suggest a way for the
interpretation of different time courses of lesion develop-
ment in DWI within a clinical MRI protocol. MR stroke
imaging delivers important information in acute stroke,
particularly in defining the ‘tissue at risk of infarction’.
Copyright © 2002 S. Karger AG, Basel
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Accepted: March 14, 2002
Multiparametric stroke imaging combining diffusion-
and perfusion-weighted magnetic resonance imaging
(DWI and PWI), magnetic resonance angiography (MRA)
and conventional magnetic resonance sequences such as
fluid attenuated inversion recovery is increasingly uti-
lized as the primary imaging modality in major stroke
centers [1–3]. Short acquisition times reduce motion arti-
facts and enable the study of acute stroke patients with
moderate cooperation. Fast image reconstruction makes
the results of MRA or PWI available within a few min-
utes. Detectability and detection rate of acute hemispher-
ical stroke are significantly higher with DWI than with
computed tomography (CT) [4, 5]. The advantage of a
multiparametric MR imaging (MRI) approach lies in the
characterization of the lesion extension and of the stroke
mechanism, thus providing a pathophysiological basis for
rational decision making. The present paper will disre-
gard present developments in other MRI techniques like
PWI and will focus solely on DWI.
Within the last decade a considerable number of stud-
ies were dedicated to the physiological background of
DWI in experimental ischemia and human stroke. The
Jens Fiehler
Department of Neuroradiology
University Hospital Eppendorf
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Martinistrasse 52, D– 20246 Hamburg (Germany)
Tel. +49 40 42803 4023, Fax +49 40 42803 6799, E-Mail fiehler@uke.uni-hamburg.de
Universität Osnabrück
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Fig. 1. Acute (3 h) and chronic (7 days)
stroke imaging of a patient who presented
with neglect and left-sided hemiparesis. The
large perfusion deficit on the PWI (time-to-
peak, TTP map) was caused by an occlusion
of the middle cerebral artery trunk (see ar-
row on MRA). The degree and duration of
the perfusion deficit were sufficient to cause
a decrease in ADC in the nucleus lentiformis
but not in the whole area of the middle cere-
bral artery. Thus, after intravenous throm-
bolysis and timely vessel recanalization, the
lesion did not grow and the acute lesions in
acute DWI and ADC map almost exactly
match the chronic lesion in fluid-attenuated
inversion recovery (FLAIR).

translation of free water molecules from the extracellular
(ECS) to the intracellular (ICS) space along with ischemic
cell depolarization is regarded as the hallmark for diffu-
sion slowing [6, 7]. Whereas numerous animal studies
were dedicated to the temporal development of acute
cerebral ischemia, human DWI data on acute stroke with-
in 6 h or less after stroke onset, the time window relevant
for thrombolytic therapy, is still limited.
A widely accepted hypothesis among clinicians ap-
plying DWI was that lesions with diffusion slowing repre-
sent tissue prone to infarction [8] even though animal
research indicated that this is not necessarily true [9].
Another hypothesis was that absolute values of the appar-
ent diffusion coefficient (ADC) might deliver a measure
of tissue viability [10]. Both hypotheses have not only
been challenged by experimental work [11, 12] but also by
recent stroke studies [13]. With increasing numbers of
DWI studies in acute stroke patients, a normalization of
initially decreased ADC values is reported in patients
with spontaneous [14–17] or therapeutic reperfusion [13].
On the other hand, reports on the absence of early DWI
abnormalities in tissue infarcted later on emerge [14, 18–
21]. Although there appears to be a relationship between
the degree of the perfusion deficit and the degree of the
ADC decrease, recovery cannot be predicted by ADC val-
ues alone in individual patients [17].
This raises questions on the value of DWI for the
detection of irreversibly damaged tissue and the reliabili-
ty of the DWI/PWI mismatch concept (fig. 1). A better
understanding of the physiological background of DWI is
crucial for the application of multparametric MRI in clin-
ical stroke. In the first place, basic mechanisms of water
diffusion in tissues and the background of DWI will be
discussed. Then, the pathophysiological mechanisms of
ADC decrease and an increase in cerebral ischemia will be
covered. Evolution of ADC in time and space will be dis-
cussed in association with the perfusion deficit and ana-
tomic localization. As a consequence of these consider-
ations, the relevance of ADC for the determination of tis-
sue viability will be reviewed. Taking the basic mecha-
nisms of water diffusion into account, we will estimate the
current potential and limitations of DWI in acute stroke
and its role within a multiparametric MRI stroke proto-
col.

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 Basic Mechanisms
Water Diffusion in Tissues
Diffusion is referred to as random microscopic motion
of water molecules. Pure water at 37 ° C diffuses at a rate
of approximately 3.00 ! 10 –3 mm2 s –1. The diffusion
coefficient is lower within tissue as compared to free
water because of the restrictions due to fibers, membranes
and macromolecules [22]. Within biological tissue, the
apparent diffusion coefficient values are different for
individual diffusion directions with more restricted diffu-
sion perpendicular to fiber tracts and faster diffusion par-
allel to tracts. This variability of the ADC as a function of
direction in space is called diffusion anisotropy and is
employed in diffusion tensor imaging for the visualization
of the intrinsic tissue architecture (e.g. fiber tracts) and its
physiological status [23].
DWI Sequences
In principle, DWI is based on the additional signal
intensity loss of phase dispersion accumulated by ran-
domly moving spins between two diffusion-sensitizing
magnetic field gradients. Thus, diffusion weighting in an
MR image reflects random motion along the direction of
the applied gradients. The strength of the applied diffu-
sion sensitization is dependent on its duration (‰) and its
amplitude (Gd). The degree of diffusion weighting can be
altered by adjusting the strength and time between the ris-
ing edges of the diffusion-sensitizing gradients (diffusion
time, ¢) and is expressed by the b-value (in human studies
typically 500–1,500 s/mm2) which is calculated by b =
Á2Gd2‰2(¢ – ‰/3), where Á represents the gyromagnetic
constant of the protons. The technical values for ‰ and ¢
cannot be chosen short enough for detection of an abso-
lute restriction-free diffusion. Thus, the measured diffu-
sion coefficient is called the apparent diffusion coefficient
(ADC). Typical ADC values in human brain are age-
dependent and range between 0.67 and 0.83 ! 10 –3 mm2
s –1 in gray (caudate nucleus and frontal cortex) and from
0.64 to 0.71 ! 10 –3 mm2 s –1 in white matter [24].
A major concern in DWI are motion artifacts especial-
ly with increasing diffusion time. Therefore, a single shot
MRI technique is utilized that accomplishes acquisition
times of 1 min for 20 slices. Disadvantages of this tech-
nique include EPI distortions, susceptibility, ghost and
chemical shift artifacts, which have to be considered in
image interpretation [for review of technical aspects of
DWI, see 25].
Recent human stroke studies typically used a standard
DWI sequence with a multislice, single shot spin-echo
DWI – Tool of Uncertain Value?
echo planar imaging sequence including 2–3 different b-
values. Typically, gradients in three orthogonal directions
are applied in order to acquire the mean diffusivity in
space independent of gradient direction (‘trace images’).
As a quantitative measure of water diffusion, a map of the
apparent diffusion coefficient is calculated pixelwise as
the logarithm of the signal intensity in dependence of the
b value [ADC = ln (S0/S1)/(b1 – b0)]. The major nondiffu-
sion effect contributing to hyperintensity in DWI is the
‘T2 shine through’ effect. This effect is due to the ‘contam-
ination’ of DW images by T2 signal hyperintensity result-
ing from lesions with T2 prolongation (i.e. vasogenic ede-
ma). Since T2 contamination does not influence quantita-
tive maps of the ADC, ADC maps are informative for the
estimation of the age of an ischemic lesion. To avoid
ambiguous information from DWI, multiparametric
diagnostic stroke imaging should include DWI and quan-
titative ADC maps and T2w images for a complete diag-
nostic evaluation.
Mechanisms of ADC Decrease and Increase in
Cerebral Ischemia
Comparably to CT, where changes of radiolucency
reflect elevated total tissue water content due to vasogenic
edema [26, 27], increased signal intensities in T2w MRI
appear approximately 2–4 h after cerebral ischemia and
are thought to reflect irreversible tissue damage. For the
ADC as a measure of diffusivity, the situation is more
complex. ADC values in acute stroke experience a typical
sequel of an early decrease [minutes to !1 h; (cell depolar-
ization and cytotoxic edema)] when T2w imaging may
still be normal, ‘pseudonormalization’ after 1–10 days
(increased extracellular water content = vasogenic edema)
followed by a further rise above normal ranges (cell lysis
and necrosis) [28, 29]. Several exceptions to this rule exist
that will be explained in the section below.
Decrease of ADC Values
Cerebral ischemia below a critical cerebral blood flow
(CBF) threshold results in the disruption of energy metab-
olism with consequent failure of ion pumps and anoxic
cell membrane depolarization. As a result of increased
membrane permeability and loss of ion homeostasis, wa-
ter shifts from the ECS into the ICS resulting in cell swell-
ing (cytotoxic edema) [30, 31].
Ischemic depolarization occurs within 2 min after
onset of experimental ischemia and coincides with a rapid
ADC decrease [32, 33]. The link between ion homeostasis
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and ADC has been shown for global cerebral ischemia
already [34] and has been confirmed by blocking the Na+
channels, which results in a delay of the rapid ADC
decrease [33]. Several reports about transient ADC de-
creases in experimental spreading depression [32, 35–
38], peri-infarct depolarizations [32, 36], hypoglycemia
[39], under electrical cortical stimulation [40, 41] as well
as observations on epileptic seizures in humans [42]
demonstrate the correlation between cell depolarizations
and ADC decreases. Multiparametric postictal and ictal
MRI detects reversible ADC changes in patients with
complex partial seizures [43]. Consequently, neuronal
activation of the occipital cortex due to visual stimula-
tion was shown to result in minute decreases of water dif-
fusion [44].
In stroke models of permanent vessel occlusion, the
progression restriction of water diffusion in the ECS is
mainly due to cellular swelling and is thought to be the
main mechanism of ADC decrease [45–49]. It has been
postulated that ADC represents the weighted average of
ECS to ICS [45], where diffusion is interfered by macro-
molecules [45, 50]. Diffusion-weighted hyperintensity is
not attributable to the cessation of blood flow and the con-
comitant fast intravascular water displacement (‘pseu-
dodiffusion’) [51] because it does not appear abruptly at
the onset of ischemia and resolves slowly in early reperfu-
sion [52]. The effects of cell volume changes on ADC are
less pronounced in cell culture than that measured for
dead cells [49]. Thus, additional mechanisms have to be
included in models for description of ADC changes: a
changed tortuosity of the paths in the ECS occurs, de-
pending on the cellular architecture [53, 54]. Alterations
in membrane permeability [55], changed cytosolic viscos-
ity [56] and cytoskeletal motility [40] have been dis-
cussed. However, a quantitative relationship between
ADC and cell volume can be described in a relatively sim-
ple equation [46, 57], the validity of which is supported by
a body of experimental work.
The relationship between ADC changes and CBF lev-
els as well as metabolic disturbances has been extensively
studied [58]. Low ADC values were found in ischemic tis-
sue with severe CBF decrease and ATP depletion as indi-
cators of the ischemic core 2 h after vessel occlusion in
rats. Moderately decreased ADC values of F90% of con-
trol were found in penumbral tissue with tissue acidosis
but without ATP depletion [58]. Accordingly, even at 2 h
after experimental vessel occlusion, the region of hyperin-
tensity in DWI was larger than that of ATP depletion and
agreed with the area of tissue acidosis [59]. Thus, the area
with hyperintensity in DWI or ADC decrease may in-
190 Cerebrovasc Dis 2002;14:187–196
clude the penumbra or in MRI terms ‘tissue at risk of
infarction’.
Water shifts from the ECS to the ICS with consecutive
cell swelling may occur at CBF levels well above the
threshold for ischemic depolarization, if moderately de-
creased CBF levels are maintained for a longer time peri-
od [60]. It is likely that an increase of the intracellular
osmolarity due to lactate accumulation from anaerobic
glycolysis is the reason for cell swelling beyond depolari-
zation [61]. These observations help to explain moderate
ADC decreases without membrane depolarization [33,
60]. On the other hand, DWI-negative stroke patients
with severe symptoms were observed [18, 62]. Obviously,
within a limited time window, penumbral tissue may
exhibit lost function but no detectable ADC reduction.
The duration and the degree of the ischemia will deter-
mine cell depolarization with ADC decrease or ADC
decrease without cell depolarization due to the above-
described mechanism of increased intracellular osmolari-
ty due to lactate accumulation from anaerobic glycolysis.
This spectrum of possible patterns mirrors the com-
plex mosaic of ADC changes in focal and global cerebral
ischemia. It is a simplification to assign ADC decreases to
cerebral ischemia in general: ADC decrease is an indica-
tor of ischemia but neither specific to irreversible tissue
damage nor decreased under all circumstances.
Recovery of ADC Values
The increase of initially decreased ADC values after
acute ischemia may be attributed to the balance of cyto-
toxic and subsequently developing vasogenic edema. Af-
ter a variable time period of 1–10 days (in humans) the
ADC approaches normal values while T2 is prolonged
indicating vasogenic edema and infarction. This ‘pseu-
donormalization’ of ADC values (normal ADC, lesion in
T2w MRI) [29, 63, 64] is attributed to increased extracel-
lular water content, the vasogenic edema, as reflected by a
signal intensity in T2w MRI and reaches supranormal
values when cell lysis and encephalomalacia occur.
The extreme temporal spread of ADC pseudonormali-
zation in humans may be explained by intralesional dif-
ferences [65] which is influenced by the severity and dura-
tion of the perfusion deficit, the presence of bleeding, the
type of the affected tissue and potentially other factors.
Vasogenic edema and cell lysis dominate around days 4–
10 [29, 66]. However, reperfusion with restoration of
blood flow within the first 24 h may lead to progressive
vasogenic edema development due to the effects of post-
ischemic blood-brain barrier disruption and reperfusion
injury [11, 28, 67]. Another cause of early ADC normal-
Fiehler et al.
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ization after short ischemic periods is tissue salvage [12],
which might be a correlate of transitory ischemic attacks
[14].
The secondary rise in ADC might be the early balance
between astrocytic swelling and neuronal retraction [68]
where no lesion in T2w imaging was observed. However,
this early normalization was associated with tissue dam-
age in later development as well. A further cause of early
secondary ADC increases is hemorrhagic transformation
especially in major strokes and after thrombolytic therapy
[69].
Evolution of ADC in Time and Space
Absolute ADC values represent a snapshot during the
course of stroke evolution. Identical ADC values may
reflect completely different physiological entities in the
ischemic cascade and may coincide with various histolog-
ical states of ischemic damage [68]. Complicating the situ-
ation even more, various stages of ADC transition may
exist side by side in adjacent cerebral regions of gray and
white matter [48, 65, 70].
In the absence of reperfusion, the core of the ischemic
lesion with the lowest ADC values spreads over time to
adjacent areas with moderately reduced ADC values in
animal research [58, 71] as well as in human stroke [72].
Peripheral areas with formerly normal ADC values are
recruited and show ADC decreases, leading to an onion
skin-like lesion growth [17]. In case of vessel recanaliza-
tion and tissue reperfusion, the time point and dynamics
of restored CBF determine the resulting changes in ADC
[11]. Whether areas with ADC decrease truly normalize
(no lesion in T2w imaging) or not depends more on the
time point of reperfusion than on the severity of the initial
ADC decrease [17].
Different patterns of time-dependent ADC changes
can be found in acute stroke. These changes may develop
in parallel during the evolution of the stroke lesion and
may either contribute to lesion growth or result in an (ap-
parent) decrease in lesion size.
Perfusion Deficit and ADC Values
The severity of the ischemic impairment (duration and
degree of ischemia) is in a way reflected by the degree of
the ADC decrease and depends on the vessel occlusion
type and the efficiency of collateral blood flow pathways.
Severe CBF reduction results in a more rapid ADC
decrease than a moderate perfusion deficit [59, 73]. The
experimentally described association between the degree
DWI – Tool of Uncertain Value?
of the perfusion deficit and the severity of the ADC
decrease during vessel occlusion [9, 58] has been con-
firmed in humans [72, 74]. Besides this dependency,
ADC values decline along with the duration of the perfu-
sion deficit [11, 12, 75].
In animal research, ADC decreases resolve permanent-
ly when perfusion is reinstalled, after 10 min of middle
cerebral artery occlusion [12, 76]. This may be analogous
to transient ischemic attacks in humans, where reversible
DWI lesions have been shown [14]. Decreased ADC val-
ues after 20-min [70], 30-min [11, 12, 75] and 60-min [11,
77, 78] vessel occlusion turned towards normal values
within 1 h after reperfusion. However, renormalized
ADC values secondarily decreased after 2.5 h, accompa-
nied by a delayed signal increase in T2w MRI [11, 12, 70,
75]. A recent animal study indicated that more subtle T2
increases may be observed much earlier when using quan-
titative T2 imaging [77]. The biphasic ADC decrease after
30 and 60 min of vessel occlusion was accompanied by a
secondary lesion enlargement [11]. After 150 min of
occlusion, a permanent and more pronounced ADC de-
crease occurred [11] coincidentally with an early lesion in
T2w, early blood-brain-barrier damage and consecutive
most pronounced lesion growth. This pattern reflects the
commonly observed course of ADC development in
stroke patients. In conclusion, the lesion pattern in DWI
and ADC maps critically depends on the severity and
duration of the cerebral ischemia (fig. 2) and on the time
point of MRI.
Localization
Regionally selective vulnerability of certain brain re-
gions to ischemia has been known for some time [79]. It
has been suggested that – beside intrinsic tissue properties
– this heterogeneity is caused by local variations in CBF
[80, 81]. During global ischemia, reductions in CBF are
more drastic in the striatum and dorsal hippocampus
than in the thalamus and substantia nigra [80, 81]. The
latter in turn seem to posses a higher intrinsic susceptibili-
ty to ischemia [70, 82].
Accordingly in animal research, within the hippocam-
pus and caudate putamen, the frequency of the occur-
rence of primary ischemia-induced ADC changes, inter-
preted as a result of deeply decreased CBF, was higher
than in the substantia nigra and thalamus [70]. Neverthe-
less, if an early ADC drop occurred in the substantia nigra
or thalamus, the reduction was profound and irreversible,
in contrast to the reversible changes in the other investi-
gated regions. The ADC recovered completely within 1 h
in the hippocampus, cortex and caudate putamen but
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 degree of perfusion deficit
Fig. 2. Cerebral ischemia results in the dis-
ruption of energy metabolism with failure of
ion pumps and anoxic cell membrane depo-
larization. Water shifts from the ECS into
the ICS resulting in cell swelling (cytotoxic
edema). The distance of a random walk of a
spin within the diffusion time (¢) depends
on the restriction of ECS. The shorter this
distance, the less pronounced is the sig-
nal loss of the ‘tagged’ proton resulting in
the typical hyperintensity in a diffusion-
weighted image and a decreased ADC. There
is a clear association between both the dura-
tion and degree of the perfusion deficit and
the severity of the diffusion impairment, re-
flected by the ADC within the first hours
after stroke onset.
only partially or not at all in the thalamus and substantia
nigra [70]. However, secondary ADC reductions, accom-
panied by significant T2 elevations and histological dam-
age, were observed in these regions after 24 h. Similar
ADC values may reflect a different water content and rate
of ischemic changes in gray and white matter [48]. Addi-
tionally, regional heterogeneity and anisotropy play an
important role for relative changes in ADC [83].
Studying anterior choroidal artery infarction, similar
heterogeneity with reversible ADC decreases exclusively
in gray matter was found in humans as well [16]. Thus,
strictly speaking, only relative changes to an (in a clinical
situation unknown) preischemic ADC value represent the
ischemic impairment.
ADC and Tissue Viability
The contribution of the two paths of neuronal death,
apoptosis and necrosis, and the role of reperfusion in the
pathophysiology of transient ischemia is still the subject
of discussion [31]. It was hypothesized that delayed dam-
age after transient metabolic recovery and recovery of the
ADC depends on secondary energy failure resulting from
192 Cerebrovasc Dis 2002;14:187–196
b
a
time after vessel occlusion
mitochondrial damage [78, 83], persistent inhibition of
protein synthesis, free radicals [11] or on apoptosis.
The degree of ADC decrease was related to the location
and extent of neuronal injury, with pronounced changes
occurring within the areas displaying the most severe his-
tological damage [84]. However, no association of an
ADC threshold with irreversible injury was found [48, 85,
86]. Thus, even with severe ADC changes, the lesion may
be reversible. However, normalization of MR parameters
(ADC, T2w) does not necessarily indicate true tissue sal-
vage. Within normal-appearing T2w regions in postisch-
emic MRI scans, a partial neuronal necrosis can be
observed [12, 87]. Surprisingly with shorter occlusion
times the average lesion size in T2w at 7 days, which is
thought to represent the vasogenic edema, can be striking-
ly smaller than the histologically determined infarct size
[11]. Even after 10 min of vessel occlusion, a partial neu-
ronal necrosis was observed in the absence of any T2w
lesion in the chronic stage [12]. Miyasaka et al. [68]
observed swelling of neuronal dendrites and astrocytic
end feet as one of the earliest changes in ischemic cerebral
damage during early ADC reduction. After reperfusion
and transient ADC normalization, they found pro-
nounced swelling of astrocytic end feet and many dark
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neurons, indicating tissue damage. Hence acute reperfu- Table 1. Factors that determine and influence acute changes in
sion-induced normalization of ADC values appeared to ADC
be a poor predictor of ultimate tissue recovery, since sec-
Factor Evidence
ondary irreversible damage may develop [11, 12, 68, 70,
86, 88–90]. experimental human
These hypotheses based on animal research can be at
ADC decrease
least partially transferred to human stroke. With throm- Duration of ischemia √ √
bolytic treatment, large ischemic lesions on DWI may Degree of ischemia √ √
transiently and permanently appear normal on follow-up Electrical activity √ √
MRI without differences in the clinical course between Spreading depression √
Lactic acidosis √
both patient groups [13]. Even if areas with reversible
Glucose level √
DWI hyperintensities tend to display higher mean ADC Localization √ √
values [91], an absolute ADC viability threshold in hu-
ADC increase
mans does not seem to exist. A complete ADC recovery Balanced cytotoxic-vasogenic edema √ √
without lesion in T2w imaging on day 7 has been found Balanced astrocytic swelling and
even within regions with initially severely decreased ADC neuronal retraction √
values (!50% of the mean contralateral value) [17]. On Hemorrhagic transformation √ √
the other hand, partial neuronal loss was depicted by Tissue recovery, permanent √ √
iomazenil SPECT in patients with prolonged perfusion
deficit in areas with normal ADC [92]. In human stroke,
the degree of ADC decreases is correlated with the isch-
emic impairment but does not predict the fate of the tis-
sue after potential reperfusion. extended towards the center of the lesion, if patients are
studied within the hyperacute stage (!6 h). Nevertheless,
despite these minor (but important) limitations, which
Conclusions have been recognized only recently and which were the
focus of this review, DWI remains a highly valuable tool
The mechanisms in diffusion-weighted imaging are on in the evaluation of acute stroke patients, especially in the
a safe ground of a considerable body of experimental first hours after symptom onset.
work. A diffusion-weighted image represents a snapshot
in stroke evolution (table 1). Marked and early ADC
decreases are correlated with a severe perfusion deficit Acknowledgment
causing energy failure whereas tissue without any change
The authors gratefully acknowledge a grant from the Bundesmi-
of ADC is less severely involved. Thus, DWI is just one
nisterium für Bildung und Forschung within the ‘Kompetenz Netz-
side of the coin and should be interpreted in the context of werk Schlaganfall’ for research on acute stroke MRI.
the time after stroke onset, perfusion and Tw2 imaging
and occlusion type. In principle, lesions in DWI are
reversible independent of the degree of the ADC decrease
within the first hours after stroke onset. ADC decreases
might be reversible especially after occlusion of minor
branches of the MCA that can be reversed by thrombolyt-
ic therapy. Most acute stroke patients will show the time
course of persistent ADC decrease during the first days if
nutritional reperfusion is not achieved timely. The con-
cept of a mismatch between the lesion volume in DWI
and PWI indicating ‘tissue at risk of infarction’ appears
valuable to estimate the prognosis in acute stroke pa-
tients. However, it has to be kept in mind that ADC
lesions are not necessarily an indicator of irreversible tis-
sue damage and the ‘tissue at risk of infarction’ has to be

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