Download Digital Map of Posterior Cerebral Artery Infarcts Associated

Digital Map of Posterior Cerebral Artery Infarcts
Associated With Posterior Cerebral Artery Trunk and
Branch Occlusion
Thanh G. Phan, MBBS, FRACP; Ashley C. Fong, MBBS;
Geoffrey Donnan, MD, FRACP; David C. Reutens, MD, FRACP
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Background and Purpose—Knowledge of the extent and distribution of infarcts of the posterior cerebral artery (PCA)
may give insight into the limits of the arterial territory and infarct mechanism. We describe the creation of a digital
atlas of PCA infarcts associated with PCA branch and trunk occlusion by magnetic resonance imaging techniques.
Methods—Infarcts were manually segmented on T2-weighted magnetic resonance images obtained ⬎24 hours after stroke
onset. The images were linearly registered into a common stereotaxic coordinate space. The segmented images were
averaged to yield the probability of involvement by infarction at each voxel. Comparisons were made with existing maps
of the PCA territory.
Results—Thirty patients with a median age of 61 years (range, 22 to 86 years) were studied. In the digital atlas of the PCA,
the highest frequency of infarction was within the medial temporal lobe and lingual gyrus (probability⫽0.60 to 0.70).
The mean and maximal PCA infarct volumes were 55.1 and 128.9 cm3, respectively. Comparison with published maps
showed greater agreement in the anterior and medial boundaries of the PCA territory compared with its posterior and
lateral boundaries.
Conclusions—We have created a probabilistic digital atlas of the PCA based on subacute magnetic resonance scans. This
approach is useful for establishing the spatial distribution of strokes in a given cerebral arterial territory and determining
the regions within the arterial territory that are at greatest risk of infarction. (Stroke. 2007;38:1805-1811.)
Key Words: middle cerebral artery 䡲 digital techniques 䡲 atlas 䡲 stroke
S
troke is the second most common cause of death and
disability worldwide and contributes to a large percentage of the global burden of disease.1 The management of
stroke depends on accurate knowledge of the arterial territory.
Delineation of the arterial territory or territories involved in
ischemic stroke can help the clinician narrow or widen the
scope of investigations. For example, carotid artery disease is
less likely to be the mechanism of occipital lobe infarcts
because this region is supplied by the vertebrobasilar system
via the posterior cerebral artery (PCA). In addition, accurate
knowledge of the arterial territory allows the distinction
between infarcts located within an arterial territory and those
located in the border zone between arterial territories to be
made, the latter suggesting an infarct mechanism related to
hypoperfusion.2
More recently, information on the spatial extent of infarction has been incorporated into therapeutic decision making
for middle cerebral artery (MCA) infarcts with respect to
thrombolysis.3 The percentage of the vascular territory (“rule
of one third”) affected by early ischemic changes has been
correlated with an increased risk of hemorrhage after administration of recombinant tissue-type plasminogen activator.3
Accurate knowledge of MCA infarct territory may aid the
clinician in determining infarct size and has enabled the
systematic analysis of other methods of assessing hemorrhage
risk, such as the ASPECTS template.4
Compared with the volume of work aimed at understanding the territory of MCA occlusion,5 relatively little emphasis
has been given to PCA infarcts, despite the fact that PCA
strokes account for 26.5% of ischemic stroke6 and the
substantial disability caused by PCA infarction, which includes visual-field defects (thus, impairing driving ability),
hemiparesis, sensory disturbances, and disturbances in cognition and behavior.6,7
Available maps of cerebral arterial territories are largely
perfusion maps based on injection studies in cadavers.8 –11
Advanced magnetic resonance (MR) perfusion imaging techniques with endogenous contrast material (arterial spin labeling) have been used to produce maps of the arterial territories.12 These territories may not be comparable with the area
Received November 4, 2006; final revision received December 21, 2006; accepted January 10, 2007.
From the Southern Clinical School, Monash University, Clayton, Australia; the National Stroke Research Institute, Heidelberg, Australia; and the
Austin and Repatriation Medical Centre, University of Melbourne, Heidelberg, Australia.
Correspondence to David C. Reutens, MD, FRACP, Southern Clinical School, Monash University, 246 Clayton Rd, Clayton, Victoria, Australia. E-mail
[email protected]
© 2007 American Heart Association, Inc.
Stroke is available at http://www.strokeaha.org
DOI: 10.1161/STROKEAHA.106.477000
1805
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Stroke
June 2007
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affected by arterial occlusion in subjects with ischemic stroke
because of the younger age of subjects used to create the
cadaver and MR perfusion maps.5,12–14 Atherosclerotic disease in stroke patients may also lead to the development of
leptomeningeal collaterals,13 which may influence the region
at risk of infarction. Hence, mapping of the arterial infarct
territory in cases of known occlusions of specific arteries may
provide a more realistic understanding of the region at risk of
infarction than do cadaver-based maps.5 The correspondence
between these mapping modalities is unknown for the PCA
but may not be close, based on our observations of MCA
infarction. Previously published maps have a limited number
of slices and may be difficult to use in clinical practice when
the site of infarction is not at the same level as the one
depicted.9 –11,15
We have created a digital probabilistic atlas of PCA
infarcts (DA-PCA) from T2-weighted MR imaging scans in
patients with occlusion of the PCA trunk and/or P1 or P2
segments on MR angiograms. This map was then compared
with existing maps of the PCA territory.
Subjects and Methods
Patient Selection
MR scans performed in our institution between January 1999 and
June 2006 with reported PCA trunk or branch occlusion on MR
angiography (MRA) were collected. The MR images were inspected
and clinical notes were reviewed. Patients were included in the study
if the images demonstrated “occlusion” of the PCA trunk (P1) and/or
P2 or P3 branches (nomenclature of Zeal and Rhoton16) on the
initial MRA, as defined by the loss of signal on the maximumintensity projection and the corresponding source images of the
MRA. T2-weighted MR scans were performed ⬎24 hours after
stroke onset.
Patients who had new or concurrent infarcts in the MCA and
anterior cerebral artery (ACA) territory were excluded. The mechanism of infarction was determined according to the Trial of Org
10172 in Acute Stroke Treatment17 criteria as large-artery atherosclerosis, cardioembolism, small-vessel occlusion, stroke of other
determined etiology, and stroke of undetermined etiology. No
patient received recombinant tissue-type plasminogen activator.
The study was approved by the human research ethics committee.
Imaging Techniques
MR imaging scans were performed on a 1.5-T superconducting
imaging system (General Electric Medical Systems, Milwaukee,
Wis, and Siemens Medical Solutions, Malvern, Pa) with echoplanar
imaging capabilities. T2 images were acquired with a thickness of
6 mm/1.7 mm; matrix size of 256⫻256; and a repetition time/
echo time/echo train length of 2000 ms/102 ms/12. The
3-dimensional time-of-flight MRA was performed with a repetition time/echo time of 38/6.9 ms; 25° flip angle; thickness of
1.4 mm; slab thickness of 60 mm; matrix size of 256⫻224; and
field of view of 180 mm.
Registration and Segmentation
Alignment of corresponding anatomic structures in images (before
segmentation) from different subjects was achieved by registration to
a standard brain template (MNI template available at http://www.
bic.mni.mcgill.ca/software/).18 Manual registration was performed
by identifying homologous internal and external anatomic landmarks
on the standard brain template and patient image. Landmarks were
individualized for each patient and were chosen with use of an
interactive display package that allowed the user to ensure that
landmark selection progressively improved image alignment. Manual registration was used rather than image intensity– based auto-
mated methods because of potential inaccuracies in the latter
introduced by the presence of a lesion. These steps led to the creation
of a 9-parameter linear transformation matrix that allowed for
rotation, translation, and scaling of the patient image along each of
the 3 principal axes.19 In a previous study that included the same
methodology, we had shown that the registration error was small.5
The registration step also had the effect of correcting for overall
differences in brain size. Segmentation was performed on the MR
scans performed ⬎24 hours after ischemic stroke onset. Cerebral
infarcts were manually segmented on T2-weighted images with the
use of interactive mouse-driven software and standardized intensity
windows.
Creation of the DA-PCA
To create a composite map, the images from subjects with infarcts in
the right hemisphere were also “flipped” along the y axis so that all
infarcts lay on the left side of the image, according to radiologic
convention. Registered binary images of the infarcts were averaged
to create the DA-PCA. Anatomic interpretation was facilitated by the
use of an existing database that related Talairach coordinates to
anatomic structures (Talairach Daemon; available at http://ric.uthsca.
edu/projects/talairachdaemon.html).20
Summary statistics were calculated for volumes obtained in
individual patients. From the probability maps, the volume of tissue
at a number of probability thresholds was calculated. The maximum
infarct volume is defined by the voxels with probabilities exceeding
the minimum probability. The mean infarct volume is defined by
the voxels with probabilities exceeding the mean probability. The
standard error of the mean of these measurements of PCA
territory infarct volume was calculated by a “leave one out” or
jack knife analysis.21 Volumes for patients with P1 (trunk)
occlusion were compared with those for P1–P3 (trunk-branch)
occlusion.
Comparison With Existing Maps
Comparisons with existing vascular territory maps were performed
both qualitatively and quantitatively. Maps chosen for comparison
were those widely cited in the literature. Maps by van der Zwan et
al,9 Beevor,10 and Tatu et al11 were based on arterial injection studies
in cadavers unaffected by stroke. The map by Damasio15 is a
composite map derived from textbooks on the cerebral circulation.
The map by Tatu et al11 provides a stylized depiction of the
variability of the arterial territory, taking into account the description of van der Zwan9 and Beevor.10 The map of van Laar et al12
is based on MR perfusion (arterial spin labeling) of the basilar
arteries and PCAs.
Results
Clinical Characteristics
There were 30 patients (24 men) with a median age of 61
years (range, 22 to 86 years). All patients had MR imaging
performed as part of the routine stroke work-up. As a result of
this protocol, the T2-weighted MR imaging scan that was used
for segmentation was performed at a median interval of 5
days (range, 1 to 224 days) after stroke onset. The stroke
mechanisms and sites of arterial occlusion are displayed in
Table 1. The mean (⫾SD) infarct volume in individual
patients was 26.2⫾22.8 cm3, and the maximum volume was
92.3 cm3. According to infarct probabilities, the mean and
maximum infarct volumes obtained from the 20 patients with
P1 occlusion and the 30 patients with P1–P3 occlusion are
shown in Table 2.
The regions with the highest probability of PCA infarction were the parahippocampal and lingual gyrus (0.60 to
0.70; Figure 1). The probability of infarction in the
posterolateral thalamus was 0.33. The probability of in-
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Digital Map of PCA-Infarct
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TABLE 1. Clinical Characteristics, Including Time of MR Scans, Severity of Neurologic Deficit, Stroke Mechanisms, and Sites of
Arterial Occlusion
Age, y
Sex
Time of MR
Scans, d
NIHSS
Score on
Admission
Infarct
Volume,
cm3
Side of
Infarction
TOAST
Classification
Ipsilateral
Fetal PCA
Vertebral
Artery
Occlusion
PCA
Trunk
Occlusion
P2
Occlusion
P3
Occlusion
37
M
2
2
53.1
Left
Unknown
⫺
⫺
⫹
⫹
⫹
29
M
5
3
20.9
Left
Unknown
⫺
⫺
⫹
⫹
⫹
29
M
4
2
16.6
Left
Unknown
⫺
⫺
⫺
⫺
⫹
34
M
2
4
69.3
Right
Unknown
⫺
⫺
⫹
⫹
⫹
67
F
5
7
22.4
Left
Unknown
⫺
⫺
⫹
⫹
⫹
77
M
84
1
2.4
Left
Unknown
⫺
⫺
⫹
⫹
⫹
61
M
37
1
6.1
Left
Unknown
⫺
⫹
⫺
⫹
⫹
51
F
1
4
0.7
Right
Unknown
⫺
⫺
⫹
⫹
⫹
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30
F
7
2
5.2
Left
Unknown
⫺
⫺
⫺
⫺
⫹
58
M
15
1
1.0
Left
Unknown
⫺
⫺
⫹
⫹
⫹
61
M
2
2
18.3
Left
Unknown
⫺
⫺
⫹
⫹
⫹
42
M
86
11
33.8
Left
Unknown
⫺
⫺
⫹
⫹
⫹
86
M
4
11
92.3
Left
Unknown
⫺
⫺
⫹
⫹
⫹
22
F
7
3
15.3
Left
Unknown
⫺
⫺
⫺
⫹
⫹
66
M
6
6
37.9
Right
Unknown
⫺
⫺
⫹
⫹
⫹
61
M
2
2
3.6
Right
Unknown
⫺
⫺
⫹
⫹
⫹
70
M
224
2
7.6
Right
Unknown
⫺
⫺
⫹
⫹
⫹
68
M
2
2
7.0
Left
Large artery
⫺
⫺
⫹
⫹
⫹
41
M
1
8
25.7
Right
Large artery
⫺
⫺
⫹
⫹
⫹
56
M
54
2
7.8
Left
Large artery
⫹
⫺
⫺
⫺
⫹
86
F
29
2
25.0
Right
Large artery
⫺
⫺
⫹
⫹
⫹
73
M
89
12
14.9
Left
Large artery
⫺
⫺
⫹
⫹
⫹
50
M
5
5
38.2
Right
Large artery
⫺
⫺
⫹
⫹
⫹
70
M
9
5
18.9
Right
Large artery
⫺
⫺
⫹
⫹
⫹
62
M
1
2
60.4
Left
Cardioembolic
⫺
⫺
⫺
⫹
⫹
39
M
1
1
6.0
Right
Cardioembolic
⫺
⫺
⫺
⫹
⫹
78
F
5
2
38.2
Left
Cardioembolic
⫺
⫺
⫺
⫹
⫹
85
M
2
2
34.3
Left
Cardioembolic
⫺
⫺
⫹
⫹
⫹
77
M
2
2
48.7
Right
Cardioembolic
⫺
⫺
⫺
⫹
⫹
64
M
2
2
53.1
Left
Cardioembolic
⫺
⫺
⫺
⫹
⫹
NIHSS indicates National Institute of Health Stroke Scale; TOAST, Trial of Org 10172 in Acute Stroke Treatment.
farction in the occipital pole varied from 0.10 inferiorly
(fusiform gyrus) to 0.43 at the level of the lingual gyrus
and 0.10 superiorly (cuneus). The regions with a low
probability of PCA infarction were the splenium (0.10),
posterior limb of the internal capsule and posterior part of
the lentiform nucleus (0.04), and tail of the caudate
nucleus (0.04). The mean and median probabilities of
infarction were 0.16 and 0.10, respectively.
TABLE 2. Comparison of PCA Territory Infarct Volumes Obtained by Using Predetermined Probability Thresholds for the DA-PCA and
for the Map by van der Zwan et al22
PCA Territory Volume
DA-PCA, P1 occlusion (n⫽20)
DA-PCA, P1–P3 Occlusion (n⫽30)
Map of van der Zwan et al22 (n⫽23)
Method
MR imaging and MRA based
MR imaging and MRA based
Cadaver
Maximal extent: voxel probability ⬎0
(mean volume⫾SD)
3
128.90.1⫾14.3 cm
3
152.6⫾43.3 cm
228.6 cm3
Maximum volume in individual subjects
Voxel probability⬎mean probability
(mean volume⫾SD)
3
55.1⫾8.7 cm
3
56.6⫾43.3 cm
118.7⫾34.7 cm3
Mean volume in individual subjects (⫾SD)
Minimum volume
⫺
⫺
69.1 cm3
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Figure 1. DA-PCA territory infarction associated with PCA trunk and branch occlusion in stereotaxic coordinate space. The probability
of infarction is displayed in color superimposed on the T1-weighted template image in stereotaxic coordinate space. The average MR
image was generated from 152 neurologically normal subjects. Slices are 10 mm apart, ranging from a z coordinate of ⫺50 to 90 mm
with respect to the line connecting the anterior and posterior commissure. The color bar refers to the frequency of infarction at each
voxel. The highest frequency of infarct occurrence is in the parahippocampus and lingual gyrus.
Comparison With Existing Maps
The maximum infarct volume of the DA-PCA was much
lower than that of van der Zwan et al22 (Table 2). The
anatomic location of the boundaries of the PCA infarct
territory in each map is provided in Table 3 and shown in
Figure 2. The maximal extent of the DA-PCA map resembles
that of Damasio15 and the minimum arterial map of Beevor10
and van der Zwan et al9 but not the maximum arterial map of
Beevor,10 van der Zwan et al,9 and Tatu et al11 because of the
lack of lateral extension in the superior and inferior aspects of
the probabilistic map. The superior extent of the map produced by van Laar et al12 is more congruent with the maximal
map by Beevor,10 van der Zwan et al,9 and Tatu et al11 than
our DA-PCA in terms of the lateral extent of the arterial
territory.
Discussion
This study provides information on the regions at risk of
infarction in the PCA territory. More accurate determination
of infarct territory should aid topographic diagnosis and assist
in formulating infarct mechanisms. As in our approach to
creating the digital atlas of MCA territory infarcts,5 we based
the identification of PCA territory infarcts on MR images
taken from patients with occlusion of this artery. One advantage of this approach is the absence of a priori constraints on
infarct size, shape, and location. The probabilistic approach
used here realistically captures the variability in infarct
location compared with earlier maps by showing the probability of infarction after PCA occlusion.
Methodologic Issues
Differences between previous maps of the PCA territory8
presumably influence the variety of injection techniques used,
overflow of injection material through anastomosing arteries,
variability in the physical properties of the injectate, and the
effect of different injection pressures on the flow of contrast
material in the case of MR perfusion maps. The MR perfusion
map by van Laar et al12 depicts perfusion of the entire
posterior circulation (basilar artery and both PCAs) rather
than individual PCA territory. The resultant map may also be
affected by overflow of endogenous contrast material through
anastomosing arteries, leading to overestimation of the arterial territory. Additionally, MR images were obtained only
from the level of the upper lateral ventricle, omitting the
lower part of the PCA territory.12 In this study, PCA occlusion was defined by MRA. Although it is possible that in
some cases PCA occlusion was incomplete and there was
trickle flow, this is not likely to have significantly affected the
results of the study, given that it is still indicative of severe
hypoperfusion. A potential concern of this study is the timing
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Figure 2. For the purpose of comparison, the DA-PCA is displayed on the left (L) hemisphere. Drawn on the right hemisphere (R) are
the maximal extent of the van Laar et al,12 (red) and Tatu et al11 (yellow) maps. The map of van Laar et al depicted here is derived from
the figure for the total population. Comparable images at a z level below 20 mm from the van Laar et al map are not available. The
map of Tatu et al incorporates only the arterial supply of the gray matter.
Vascular Anatomy of the PCA
of the MR scans and the effect of infarct shrinkage on the size
of the infarct territory. Although the majority of patients had
their scans performed within 5 days of stroke onset, there
were 3 patients whose scans were performed at 3 months and
1 patient whose scans were performed at 224 days. This
patient had a small stroke (7.6 mL). Even allowing for
shrinkage in infarct volume, it would not have affected the
result of this study.
TABLE 3.
We briefly summarize the origin and branches of the PCA
according to the nomenclature of Zeal and Rhoton.16 The
PCA originates from the basilar artery. Its proximal (P1) and
distal (P2) segments are defined by the posterior communicating artery.16 The proximal P1 segment is hypoplastic in
17%, in which case the P2 and its branches arise from the
anterior circulation via a large posterior communicating
Differences in PCA Territory Boundaries Between the DA-PCA and Other Published Maps
No.
Age, mean (range), y
DA-PCA
van der Zwan et al9
Tatu et al11
Beevor10
Damasio15
van Laar et al12
N⫽30
N⫽23
NA
N⫽87
NA
N⫽115
61 (22–86)
48 (15–100)
NA
NA
NA
58
MR imaging and
MRA based
Cadaver injection
Cadaver injection
Cadaver injection
Combined maps from
in vivo cerebral
angiographic studies
MR perfusion by
arterial spin
labeling
Superior and lateral
Extends to superior
occipital sulcus but
spares superior
parietal lobule
Superior parietal
lobule
Superior parietal
lobule
Superior parietal
lobule
Superior parietal
lobule
Superior parietal
lobule
Lateral and inferior
Does not extend to
superior temporal
sulcus
Extends to superior
temporal sulcus
Extends to superior
temporal sulcus
Extends to superior
temporal sulcus
Extends to superior
temporal sulcus
NA
Method
NA indicates that the axial slice at this level is unavailable for comparison. Data on the inferior extent of the PCA territory is unavailable in the map by
van Laar et al.12
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artery (fetal PCA variant).16 In the majority of cases, the P1
segment divides into the thalamoperforating arteries (to the
thalamus), ventricular and choroid plexus branches (posterior
choroidal arteries), and brainstem branches (short and long
circumflex arteries). The P2 segment divides into the posterior or inferior temporal (branches include the anterior,
middle, posterior, common temporal, and hippocampal arteries) artery and internal occipital arteries (calcarine and
parieto-occipital branches). The P2 segment also branches to
the thalamus, such as the thalamogeniculate arteries. The P3
segment begins at the posterior aspect of the midbrain, and
the P4 segment, at the anterior part of the calcarine fissure.16
The most common discrepancy between our map and those
of previous studies was the superolateral and inferolateral
extent of the PCA infarcts compared with those in cadaver
maps.11,15,22 This is in accord with the smaller territorial
infarct volume in this study compared with the perfused
regions in cadaver studies. This discrepancy may be related to
the pattern of collateral blood supply. Brozici et al14 and
Liebeskind23 have highlighted the possible relation between
the leptomeningeal collateral blood supply and variability in
the extent of stroke. These regions of low probability of
infarction correspond to regions of leptomeningeal collateral
blood supply depicted in perfusion maps.
The DA-PCA map extends as far superomedially as the
cuneus and precuneus (probability⫽0.10). The map by Tatu
et al11 depicts the leptomeningeal blood supply by the PCA
and ACA to this region. Despite the fact that in a cadaver
study7 this region was found to have received the majority of
its blood supply from the parieto-occipital artery, the relatively low probability of infarction involving this region is
possibly due to anastomoses with the posterior pericallosal
artery (branch of the ACA via the pericallosal artery).14,24,25
Unlike the cadaver9,10 and MR perfusion12 maps, the PCA
infarct territory did not extend as far laterally as the superior
parietal lobule in any patient. The map by Tatu et al11 depicts
a variable leptomeningeal blood supply by the PCA and
MCA to this region. Anastomoses are likely to form between
the parieto-occipital artery (branches of the PCA) and the
angular artery or anterior and posterior parietal arteries
(branches of the MCA).14,24,25 Inferiorly, the lack of lateral
extension to the middle temporal and lateral occipital gyri in
the digital map compared with published maps is likely to be
due to anastomoses between the anterior and/or middle
temporal arteries (branch of the PCA) and the middle and/or
posterior arteries (branches of the MCA).24 The presence of
this leptomeningeal collateral network among the branches of
the PCA7 and, to a lesser extent, from the MCA depicted by
Tatu et al11 and van der Zwan et al9 may also explain the
lower frequency of infarction in the occipital pole after PCA
occlusion (probability⫽0.12 to 0.41). This area receives its
blood supply from several branches of the PCA, such as the
calcarine artery, the parieto-occipital artery, and/or the posterior temporal artery7,26 and, to a lesser extent, from the
MCA via the temporo-occipital artery.26
At the level of the corpus callosum, the infrequent involvement of the splenium (probability⫽0.10) is possibly due to
the splenial artery (branch of the parieto-occipital, calcarine,
or medial posterior choroidal artery) forming interarterial
anastomoses with branches of the pericallosal artery (branch
of the ACA).24 Similarly, the PCA (likely via the posterior
choroidal arteries) has been described to perfuse the posterior
limb of the internal capsule and the posterior part of the
lentiform nucleus.9,11 However, the low risk of infarction in
this region due to PCA occlusion suggests that this risk is
modified by branches of the lenticulostriate arteries, which
dominate the vascular supply of this region.27
Collateral-Poor Zone
In the DA-PCA, the highest probability of involvement was
in the parahippocampus and medial occipital lobe (probability⫽0.60 to 0.70). This area is supplied by the hippocampal
artery, the posterior temporal artery, or the common temporal
artery (branches of the PCA).7 Branches from the MCA or
ACA have not been described to supply this area. The MCA
maps by Beevor,10 Tatu et al,11 and van der Zwan et al9 and
our DA-MCA5,12–14 do not extend to this area, suggesting that
the higher probability of infarction is a consequence of the
lack of collateral blood supply in this region.16 Collaterals
from the ACA or MCA supplying this area have not been
described. PCA infarction commonly involves the posterolateral thalamus (probability⫽0.33), presumably from a lack of
perfusion of the thalamogeniculate branches.
In conclusion, we have created a DA of PCA territory
infarction with the use of MR imaging techniques. The
DA-PCA can be used to objectively define the regional risk
of infarction and has been compared with existing maps of
the PCA territory, as well as current knowledge of collateral
supply. This approach may be useful to establish the distribution of the PCA and other arterial territories and the border
zones between them.
Disclosures
None.
References
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2. Bladin CF, Chambers BR. Clinical features, pathogenesis, and computed
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Digital Map of Posterior Cerebral Artery Infarcts Associated With Posterior Cerebral
Artery Trunk and Branch Occlusion
Thanh G. Phan, MBBS, FRACP, Ashley C. Fong, Geoffrey Donnan and David C. Reutens
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Stroke. 2007;38:1805-1811; originally published online May 3, 2007;
doi: 10.1161/STROKEAHA.106.477000
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