REVIEW ARTICLE

Neuroimaging in Acute Posterior Cerebral Artery Infarction
Pasquale F. Finelli, MD

Background: The role of neuroimaging in acute posterior cerebral
artery (PCA) territory infarction is less well appreciated compared
with the anterior cerebral circulation because PCA infarction occurs
less frequently and more often is associated with limited neurologic
deficit not qualifying for thrombolytic therapy. On occasion, however, hemiparesis and/or visual field defect accompanies PCA infarction that would warrant thrombolytic therapy.
Review Summary: As neuroimaging plays a central role in the
diagnosis and treatment of acute stroke in the thrombolytic era, a
series of case studies is presented to illustrate the role of computed
tomography and magnetic resonance imaging in the setting of acute
PCA infarction.
Conclusion: Familiarity with the neuroimaging features of acute
PCA infarction can facilitate management in those select patients
that qualify for thrombolytic therapy.
Key Words: thrombolytic therapy, MR imaging, CT scan,
posterior cerebral artery infarction, neuroimaging

branches supply the cerebral peduncles and lateral thalamus
and more distal branches that supply the cerebral cortex.5 The
polar artery arising from the posterior communicating artery
(PCOM) is unique in that its blood supply may come alternatively from the anterior or posterior circulation to supply
the frontal most area of the thalamus. Variant circulation is
noted particularly with a dominant PCOM (ie, fetal-type
PCA) as seen in 20% to 30% of patients where the internal
carotid artery is the principle blood supply of the PCA, and
paramedian perforators that occasionally originate from a
common trunk (Percheron’s artery) to supply the upper midbrain and both thalami.1 Depending on the location of the
vascular obstruction, any combination of midbrain, thalamus,
and PCA supplied cerebral hemisphere may be involved by
PCA stroke. The most common pattern is hemispheric involvement followed by thalamus and hemisphere, followed
by isolated thalamus, and lastly a combination of midbrain,
thalamus, and/or hemisphere.

(The Neurologist 2008;14: 170 –180)

STROKE MECHANISM AND
CLINICAL FEATURES

T

he etiology, pathogenesis and clinical features of posterior
cerebral artery (PCA) infarction are well described,1–3 yet
the neuroimaging is less well appreciated compared with the
anterior cerebral circulation. As neuroimaging plays an ever
increasing part in the diagnosis and treatment of cerebrovascular disease, a series of case studies is presented (Table 1) to
illustrate the role of computed tomography (CT) and magnetic resonance (MR) imaging in the setting of acute PCA
infarction (Figs. 1–14).

ANATOMIC CONSIDERATIONS
The paired PCA arteries are formed by the bifurcation
of the basilar artery and are the main blood supply to the
uppermost midbrain, thalamus, and posterior inferior portions
of the cerebral hemispheres, including the occipital lobes, the
medial and inferior temporal lobes, and the inferior medial
parietal lobes.4 The first portion of the PCA artery is the P1
segment whose branches supply the medial midbrain, hypothalamus, and thalamus, followed by the P2 segment whose
From the Department of Neurology, Hartford Hospital and University of
Connecticut School of Medicine, Hartford, Connecticut.
Reprints: P. F. Finelli, MD, Hartford Hospital, 80 Seymour Street, Hartford,
CT 06102-5037. E-mail: pfinell@harthosp.org.
Copyright © 2008 by Lippincott Williams & Wilkins
ISSN: 1074-7931/08/1403-0170
DOI: 10.1097/NRL.0b013e3181627679

170

The etiology of isolated PCA territory infarction most

Depending on the location of the vascular
obstruction, any combination of midbrain,
thalamus, and posterior cerebral artery supplied
cerebral hemisphere may be involved by
posterior cerebral artery stroke.

commonly is cardioembolic.1 However, involvement of the
cerebellum or brainstem in association with PCA infarction
more commonly is due to vertebral or intracranial vertebrobasilar artery disease.1 The diverse areas of brain supplied by
the PCA that include brainstem, thalamus, and cerebral hemisphere account for the protean clinical and neuroimaging
manifestations. The 3 most frequent and prominent symptoms and signs of PCA infarction are visual field defect
(95%), most commonly homonymous hemianopia, paresthesias (40%), and headache (50%). Distinct from middle cerebral artery (MCA) infarction, in PCA territory infarcts, patients are usually aware of their visual loss, and in many
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Neuroimaging in Acute PCA

TABLE 1. Case Vignettes
Case 1.

Case 2.

Case 3.

Case 4.

Case 5.

Case 6.

Case 7.

Case 8.

Case 9.

Case 10.

Case 11.

Case 12.

A 70-yr-old woman presented with a 2-d history of left-sided numbness and left visual field defect. EKG was normal and TTE showed a
patent foramen ovale and TEE showed an interatrial septal wall aneurysm.
Fig. 1. Right PCA infarction (thalamus/hemisphere) on DWI (A, B) with negative initial CT. MR shows the advantage of DWI for
location and extent of lesion.
A 83-yr-old woman presented with several days of confusion on a background of 1 yr of forgetfulness. Her recent memory and
calculations were impaired, and she did not know the name of the governor of the state. She had a visual field impairment, and the
diagnosis of progressive dementia was considered.
Fig. 2. Left PCA infarction (thalamus/hemisphere) on DWI (A, B) with negative initial CT. Her symptoms mostly resolved at 6 wk.
Alzheimer disease was considered until PCA infarction was seen. MR shows the advantage of DWI for location and extent of lesion in
a patient primarily with neuropsychological features.
A 70-yr-old woman who presented with sudden right-sided weakness and sensory loss with right homonymous hemianopia and impaired
recent memory was treated with IV tPA.
Fig. 3. Neuroimaging shows dense vessel sign on CT (A arrowhead), left PCA infarction (thalamus/hemisphere) on DWI (B) and left P2
segment PCA occlusion on CTA (C arrowhead) with recanalization by MRA and CTA (D, E).
A 75-yr-old man awakened with right arm numbness and right leg weakness that improved over 24 h. CT at an outside hospital was
normal and carotid Doppler showed a preocclusive left internal carotid artery stenosis. Warfarin was started but patient developed right
hemiparesis, aphasia, and left gaze preference.
Fig. 4. Left PCA infarction (thalamus/hemisphere) on DWI (A) with preocclusive left internal carotid artery stenosis MRA (left), CTA
(right) (B arrowheads) and fetal-type PCA on left, MRA (C arrowhead). Repeat DWI (D) showed progression of infarction. Heparin
may have been a better choice in the short term. Imaging shows role of the carotid artery in PCA infarction with fetal-type circulation
and value of CTA and MRA in delineating the vascular anatomy.
A 20-yr-old woman presented to ER with a 3-d history of double vision and droopy right eyelid, sleepiness, and unsteady gait. She was 3 mo
postpartum, smoked 1/2 pack of cigarettes/d and was treated with Depoprovera. TTE showed a PFO with aneurysmal wall dilatation.
Fig. 5. Discrete circular shaped lesion of right hypothalamus and thalamus seen on CT and DWI (A) most likely is an infarction in a
thalamoperforate artery. Follow-up MR at 1 mo showed almost total resolution of the lesion. The circular appearance of this infarct
leads to the misdiagnosis of neoplasm by several vascular specialists.
A 70-yr-old man presented with transient 30 min of numbness of left side of tongue and mandibular region. Next day he had a
recurrence including numbness of fingers of the left hand and weakness of the left leg. A TTE was negative.
Fig. 6. CT on admission was normal. DWI (A, B) study showed a discrete infarct of the right cerebral peduncle and thalamus.
A 76-yr-old woman admitted with left sided numbness and tingling and difficulty seeing on the left side. Examination showed a dense
left hemiparesis and left homonymous hemianopsia. Patient was treated with IV tPA. Repeat EKG showed atrial fibrillation and carotid
Doppler showed a right carotid occlusion.
Fig. 7. CT (A) at 2 h was negative and DWI (B) at 24 h showed a right PCA infarction (thalamus/hemisphere). MRA (C) of the neck
confirmed the right carotid bifurcation occlusion and MRA (D arrowhead) of the head showed evidence of a right P2 segment PCA
occlusion and no evidence of fetal-type PCA. This case illustrates the valve of neuroimaging when PCA infarction mimics MCA
infarction.
A 71-yr-old man with prior stroke was admitted with 1 wk history of word-finding difficulty and memory problems. A TTE showed PFO
with an interatrial septal aneurysm.
Fig. 8. Left thalamic infarction in the distribution of the polar artery that arises from the PCOM artery. Imaging delineates the vascular
anatomy of fetal PCA with hypoplastic P1 segment on MRA (B arrowhead) and infarction location on CT (A) and DWI (C).
A 74-yr-old woman transferred from outside hospital with decreased consciousness and acute myocardial infarction following chest pain
and syncope. She followed 1-step commands and drifted off. There was a suggestion of a left visual field defect.
Fig. 9. Right PCA (thalamic/hemisphere) and bilateral thalamic infarctions, initial CT (A) negative, DWI (B–D) positive. Decreased level
of consciousness without hemiparesis with a suggestion of field defect and negative early CT suggests bilateral thalamic infarction as
seen on DWI.
A 63-yr-old man was admitted with the new onset of a right visual field defect. EKG was consistent with atrial fibrillation.
Fig. 10. CT (A, B) showed left temporal tip decreased attenuation. FLAIR (C) showed the temporal tip lesion to be old (probable
arachnoid cyst) and DWI (D) identified a new area of acute infarction in the left PCA territory. Imaging illustrates how MR sequences
help with the diagnosis by determining the age of a lesion.
A 75-yr-old man was admitted with a right upper extremity seizure. One year ago, he suffered bilateral occipital infarction and 8 mo ago
was diagnosed with lung cancer.
Fig. 11. Neuroimaging showed a left occipital hypodensity on CT (A) and DWI (B) and increased signal on FLAIR (C) reported to be
consistent with infarction. A subsequent T1-weighted enhanced MR (D, E arrowhead) showed a ring-enhancing lesion consistent with
metastasis. Vasogenic edema can be appreciated on the unenhanced images.
A 75-yr-old woman collapsed in church and admitted to an outside hospital with a left hemiparesis and a right gaze deviation. CT at 1 h
showed bilateral occipital lobe decreased attenuation. EKG showed new atrial fibrillation. She was treated with IV tPA and transferred
to our hospital.
Fig. 12. Bilateral PCA territory with decreased attenuation, CT (A), early changes of a right MCA territory infarction, CT (B) and an
acute right MCA infarction, DWI (C), FLAIR (D, E), and ADC (F). The bilateral PCA infarctions were old and the right MCA
infarction new. Neuroimaging demonstrates the advantage of DWI, FLAIR, and ADC sequences over CT in distinguishing between
acute and chronic infarctions.
(Continued)

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TABLE 1. (Continued)
Case 13.

Case 14.

A 49-yr-old man was admitted with slurred speech and a right sided weakness and a right homonymous hemianopia. He was treated with
IV tPA.
Fig. 13. Neuroimaging shows dense left PCA P2 segment, CT (13 arrowhead) and absent left PCA with a fetal-type right PCA, CTA
(B arrowhead, arrow), with mismatch in the left PCA territory infarction, CTP (CBV, CBF, MTT) (C–E). Color scale of the CTP
images indicate the state of cerebral perfusion where blue represents a decrease in cerebral blood flow (CBF) and prolonged mean
transit time (MTT) (D, E) more so than the decrease in cerebral blood volume (CBV) (13C). Left PCA infarction was seen, DWI (F)
with recanalization of the left PCA, MRA (G).
A 62-yr-old woman presented with an 18 h history of left arm and leg numbness and weakness. Neurologic examination showed mild
motor and sensory deficits confined to the extremities on the left. Electrocardiogram showed new onset of atrial fibrillation and MR
imaging showed evidence of recent proximal PCA infarction. She was anticoagulated and discharged after 3 d without deficit.
Fig. 14. Neuroimaging shows restricted diffusion in the distribution of the right ATA (A–C) and thalamostriate arteries (D), and proximal
occlusion of the right PCA on MRA (E arrowhead).

DWI indicates diffusion-weighted image; PCA, posterior cerebral artery; EKG, electrocardiogram; TTE, transthoracic echocardiogram; TEE, transesophageal echocardiogram;
WNL, within normal limits; PFO, patent foramen ovale; IV tPA, intravenous tissue plasminogen activator; CTA, CT angiography; CTP, CT perfusion; MRA, MR angiography;
FLAIR, fluid attenuation inversion recovery; ADC, acquired diffusion coefficient; PCOM, posterior communicating artery; ATA, anterior temporal artery.

FIGURE 2. Left PCA infarction.

FIGURE 1. Right PCA infarction.

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patients the only accompanying symptoms are hemisensory.1
Hemiparesis is uncommon and when present is mild and
transient. Neuropsychological abnormalities associated with
PCA infarction are varied and include, memory dysfunction
followed by aphasia, dyslexia, dyscalculia, color anomia,
disorientation, visual agnosia, and palinopsia, seen in up to
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Neuroimaging in Acute PCA

FIGURE 3. Left PCA infarction.

FIGURE 4. Left PCA infarction.

32% of patients.6,7 Thalamic infarction particularly when
bilateral may be associated with profound lethargy.

NEUROIMAGING FEATURES
Much has been written about the neuroimaging in

As with middle cerebral artery territory stroke,
computed tomography may show a dense
vessel sign of the basilar or posterior cerebral
artery as the earliest feature of posterior
circulation stroke.

cerebrovascular disease, mostly in regard to the internal
© 2008 Lippincott Williams & Wilkins

carotid artery and MCA, the arterial territories most commonly involved in stroke. The PCA, the second most common arterial territory involved in cerebral infarction, accounts
for some 25% of ischemic strokes5,8 and can have similar
neuroimaging applications in the acute stroke setting (Table 2)
as described with MCA territory infarction. The diagnosis of
stroke is primarily clinical and the principle goal of neuroimaging in acute stroke management is to determine suitability for
intravenous thrombolytic therapy by excluding a nonischemic
cause of the patient’s symptoms and determining whether there
is salvageable brain.10 In select centers, with resources and
physician expertise in interventional studies, the role of imaging
is extended to identify cerebral thromboembolism amenable to
interventional therapy such as intra-arterial (IA) thrombolytic
therapy and/or mechanical clot retreival.11 Neuroimaging features apart from those directly related to thrombolytic therapy
that contribute to the overall understanding of the various aspects of PCA infarction as mechanism, etiology, and response to
therapy are noted (Table 2).

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The Neurologist • Volume 14, Number 3, May 2008

FIGURE 5. Right thalamic infarction.

Neuroimaging now plays a central role in hyperacute
stroke management and its availability in many medical
centers includes CT imaging with CT angiography (CTA)
and CT perfusion (CTP), and increasingly MR imaging with
MR angiography (MRA) without and with contrast enhancement (CE MRA), diffusion-weighted imaging (DWI), and to
a lesser extent MR perfusion. Familiarity with these modalities can provide the information necessary in the urgent
management of PCA infarction and obviate the need for more
invasive procedures as conventional cerebral angiography.
Echocardiography, transcranial, and carotid artery doppler
studies, an integral part of the evaluation of cerebrovascular
disease, are not considered here.
CT, the most widely and readily available modality for
brain imaging, may not show parenchymal changes for several hours after stroke onset, the time most critical for
initiation of stroke therapy. Nevertheless, as with MCA
territory stroke, CT may show a dense vessel sign of the
basilar or PCA12 as the earliest feature of posterior circulation
stroke (cases 3 and 13). This CT sign is due to a calcific
embolus or in situ atherothrombosis or a thromboembolic
clot. CTA serves a similar role to that of MRA, however, only
CE MRA depicts vessel anatomy with clarity similar to that
of CTA. Recently, with high-field-strength MR imaging, 3D
TOF-MRA with sensitivity encoding at 3T has resulted in
substantial improvement of spatial resolution and advanced
MRA as a reliable noninvasive diagnostic tool for the detection of steno-occlusive disease of major intracranial arteries13; however, this technology has limited availability at
present. CTA does, however, involve ionizing radiation and

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FIGURE 6. Right thalamic/peduncular infarction.

the risk of contrast induced nephropathy which is largely
offset by sodium bicarbonate nephroprotection. In the acute
stroke setting CTA assesses for stenosis, occlusion and
plaque morphology of both the vertebrobasilar and internal
carotid arteries as well as for arterial dissection and intracranial steno-occlusive and thromboembolic disease14 amenable
to interventional modalities such as IA thrombolytic therapy
and mechanical clot retrieval. Further, vessel wall calcification and anatomy with collateral and variant circulation that
may relate to the PCA are defined. Arterial dissection involving the PCA is a rare cause of infarction of this arterial
territory and has been demonstrated on MRA.15
A difference of opinion exists concerning the imaging
modality of choice in hyperacute stroke evaluation, ie, MR
versus CT. MR is favored by some16 while a trend toward a
“triple study” of CT, CTA, and CTP (total time ⬃15 minutes)
is recommended by others.9 A recent comparative study of
CTA/CTP to MR gave comparable results when used to
select stroke patients for thrombolytic therapy.17 Features
favoring CT include: (1) less time consuming, (2) relative
lack of contraindications, (3) more readily available in emergency department setting, (4) monitoring patient in CT room
is easier, and (5) CT is generally less costly than MR.
Nevertheless, individual institutional resources, expertise and
particular patient needs might support the use of MR.
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Neuroimaging in Acute PCA

FIGURE 7. Right PCA infarction.

FIGURE 8. Left thalamic infarction.

FIGURE 9. Bilateral PCA infarction.

FIGURE 10. Left PCA infarction.

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The Neurologist • Volume 14, Number 3, May 2008

FIGURE 11. CNS metastasis.

FIGURE 12. Bilateral PCA and right MCA infarction.

CE MRA can provide additional details of vascular
anatomy and along with CTA show aspects of the cerebral
vasculature previously only appreciated with conventional
angiography. Additionally, both MRA and CTA play a role in

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evaluating vessel patency to assess efficacy of thrombolytic
therapy with arterial recanalization (cases 3 and 13).
CTP, which also requires iodinated contrast, but with
possibly wider availability than MR perfusion can demon© 2008 Lippincott Williams & Wilkins

The Neurologist • Volume 14, Number 3, May 2008

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FIGURE 13. Left PCA infarction.

FIGURE 14. Right PCA infarction.

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TABLE 2. Neuroimaging Features of PCA Infarction
CT*
CT
CTA
CTP
MR
DWI
MRA
FLAIR
ADC
Enhanced
Perfusion

Lesion morphology and location, dense vessel sign (basilar and PCA)
Vessel anatomy, variants, occlusion, recanalization, dissection, plaque
morphology, and wall calcification
Evidence of infarct before CT visualization and evidence of mismatch

(Cases 3, 5, 8, and 13)
(Cases 3 and 13)

Lesion morphology, location, extent, and age

(Cases 1, 2, 5, 6, 8–10,
12, and 14)
(Cases 2, 4, 7, 8, 13,
and 14)
(Cases 10 and 12)
(Cases 10 and 12)
(Case 11)

Vessel anatomy, variants, occlusion, recanalization, and dissection,
(contrast enhanced more competitive with CTA)
Lesion morphology, location, extent, and age
Lesion age
Differential diagnosis of neoplasm, abscess, granulomatous disease, and
others
Evidence of mismatch

(Cases 13)

Italics indicate the preferred imaging modality (both italicized if no clear advantage).
*Indicates current preferred modality for acute stroke evaluation.9

strate not only changes of infarction before conventional CT
but also provide information on salvageable brain, which
represents a difference or “mismatch” between the infarct
core and surrounding ischemic penumbra, and is thus helpful
in deciding on thrombolytic therapy18,19 (case 13). A decrease in cerebral blood flow and prolongation of mean transit
time vis-à-vis a lesser decrease in cerebral blood volume
defines mismatch (case 13) and correlates with the potential
efficacy of thrombolytic therapy.20
A principle feature of DWI in stroke is its ability to
detect infarction early, frequently within an hour of symptom
onset and define the location and extent of infarction more
accurately than CT (cases 1, 2, and 6). Despite these early
changes with DWI, the CT triple study is favored (see above)
as the modality of choice in evaluating acute stroke patients
for thrombolytic therapy. Also, appreciation of lesion morphology with CT and more so with DWI can be helpful, such
that the circular appearance frequently seen with thalamic
infarction compared with the wedge shaped infarction of the
cerebral hemisphere, a result of vertical versus horizontal
vessel orientation, may avoid misdiagnosis of neoplasm,
particularly with an isolated lesion (case 5). Further, utilization of DWI, FLAIR, and acquired diffusion coefficient MR
sequences, can determine the acute, subacute, or chronic
nature of the infarction (case 10). A patient diagnosed initially by CT as bilateral PCA infarction subsequently had
DWI, acquired diffusion coefficient, and FLAIR images that
demonstrated an unsuspected recent right MCA infarction
whereas the PCA infarctions seen on CT were chronic (case
12). This case illustrates how determining infarct age can be
helpful and also show how PCA infarction may be asymptomatic. Given their common origin from the basilar artery,
infarction of the PCA occasionally is bilateral and may be
associated with a syndrome of denial of blindness (Anton
syndrome) or visual attention deficits with normal visual
fields, optic ataxia and ocular apraxia (Balint syndrome) and
lethargy if both thalami are involved (case 9).
At present, the use of thrombolytic and other interventional procedures for stroke involve the carotid, MCA, and

178

vertebrobasilar arteries where the potential neurologic disability justifies the cost and risk of the procedure.21,22 Although the same use guidelines and applications apply for
PCA infarction,8 thrombolytic therapy, both IV and IA and
other interventional procedures, are less well established, in
part because the neurologic deficits may be more limited.
Regarding isolated visual field defect from acute PCA infarction, currently there are no specific recommendations. However, considering the potential disability the consensus is to
treat with IV tPA, weighing factors as patient age, comorbidities, and lifestyle. Hemiparesis, however, may be a prominent accompaniment of PCA infarction23,24 with sufficient
stroke deficit to warrant IA thrombolytic or other interventional therapy. Interventional options should be considered
specifically when hemiparesis, particularly in association
with a visual field defect, is present in the context of a
fetal-type PCA, where the anterior circulation is the involved
vascular territory. As safety and efficacy of interventional
procedures of the posterior circulation for vertebrobasilar
artery disease become established, so to more distal intervention for the PCA territory infarction is a consideration, as
recently reported with IA thrombolysis.25
In a fetal-type PCA, the carotid system may be the main
blood supply of the PCA. In this circumstance, MRA visualization of the carotid artery including the bifurcation in the
neck and its contribution to the PCA can help correlate
clinical features. Two patients with fetal-type PCA, one of
whom had significant carotid bifurcation disease (case 4),
demonstrate the superiority of CTA compared with MRA in
this setting, and the second with a PCOM polar artery
infarction of the anterior thalamus (case 8) illustrates the
value of MRA in depicting vessel anatomy. A third patient
who presented clinically as an MCA territory infarction with
a negative admission CT, on follow-up CT showed a PCA
infarction in association with an ipsilateral internal carotid
artery occlusion on Doppler study that suggested a possible
fetal-type PCA. A subsequent DWI and MRA showed no
variant circulation, but rather a PCA occlusion with infarction
that clinically mimicked MCA territory infarction (case 7).
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Neuroimaging in Acute PCA

FIGURE 15. Cortical branches of PCA
with common variations. Reprinted with
permission from Neuroradiology.26

On occasion, PCA infarction can mimic the clinical features
of an MCA infarction particularly when hemiparesis is prominent, the result of peduncular23 or more superficial or cortical
PCA infarction.24
Another unusual occurrence is isolated infarction of
the anterior temporal artery (ATA) the most proximal
cortical branch of the PCA (case 14). The ATA arises
either from a single trunk or as multiple branches from the
proximal ambient segment of the PCA and occasionally
from the posterior temporal artery (Fig. 15). The artery
extends laterally and anteriorly beneath the hippocampal
gyrus to supply the inferior aspect of the anterior portion
of the anterior temporal lobe.26 The clinical deficits of our
patient were most likely not related to the ATA infarct but
due to the small right thalamic infarction involving the
thalamostriate arteries.
Among conditions with a predilection for the PCA
territory that can mimic infarction are infections such as
progressive multifocal leukoencephalopathy and toxoplasmo© 2008 Lippincott Williams & Wilkins

Among conditions with a predilection for the
posterior cerebral artery territory that can
mimic infarction are progressive multifocal
leukoencephalopathy and toxoplasmosis as well
as reversible posterior leukoencephalopathy and
thalamic infarction due to deep cerebral vein
thrombosis.

sis as well as reversible posterior leukoencephalopathy and
thalamic infarction due to deep cerebral vein thrombosis.
Neoplasms both primary and metastatic may mimic PCA
infarction and MR features, more than CT, are helpful in the

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differential diagnosis by demonstrating vasogenic edema and
contrast enhancement (case 11). Also, subacute infarction of
the PCA may appear as an arterial venous malformation
mimic on contrast enhanced CT.27

ACKNOWLEDGMENT
The author wishes to acknowledge Kevin Hagan for
technical assistance with image preparation.
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