Anterior cerebral artery infarction
Stroke mechanism and clinical-imaging study in 100 patients
Suk Y. Kang, MD
Jong S. Kim, MD, PhD
Address correspondence and
reprint requests to Dr. Jong S.
Kim, Stroke Center and
Department of Neurology,
Asan Medical Center, Song-Pa
PO Box 145, Seoul 138-600,
Korea
jongskim@amc.seoul.kr
2386
ABSTRACT
Background: Stroke mechanisms and clinical features of anterior cerebral artery (ACA) territory
infarction have rarely been investigated using MRI.
Objectives: To verify stroke mechanisms and to make clinical imaging correlation.
Methods: Clinical, MRI, and angiographic findings of 100 consecutive patients with ACA infarc-
tion were studied.
Results: Motor dysfunction (n ⫽ 91) was the most common symptom, and severe motor dysfunc-
tion was related to supplementary motor area/paracentral lobule involvement (p ⫽ 0.016). Hypob-
ulia/apathy (n ⫽ 43) was related to involvement of fontal pole (p ⫽ 0.002), corpus callosum/
cingulate gyrus (p ⫽ 0.003), and superior frontal gyrus (p ⬍ 0.001), and occurred more frequently
in patients with bilateral lesions followed by left lesions. Urinary incontinence (n ⫽ 30) was not
related to any specific lesion locations. Grasp reflex (n ⫽ 25) was related to corpus callosum
involvement (p ⫽ 0.035). Angiographic (mostly MR angiography) results showed that 68 patients
had local ACA atherosclerosis, most often at A2 segment. The stroke mechanisms included car-
diogenic embolism in 10, internal carotid artery–ACA embolism in 6, and ACA atherosclerosis in
61 patients. In the latter group, detailed stroke mechanisms included local branch occlusion (n ⫽
20), in situ thrombotic occlusion (n ⫽ 20), artery-to-artery embolism (n ⫽ 12), and a combination
(n ⫽ 9). Patients with intrinsic ACA disease more often had hypobulia (p ⫽ 0.077) and corpus
callosal involvement (p ⫽ 0.016) than those with embolism either from the internal carotid artery
or the heart.
Conclusion: Anterior cerebral artery (ACA) atherosclerosis is the most important stroke etiology
in our population, causing infarction with various mechanisms. Topographic lesion patterns and
consequent clinical features of ACA infarction are determined by diverse pathogenic mechanisms
and the status of collateral circulation. Neurology® 2008;70:2386–2393
GLOSSARY
A-com ⫽ anterior communicating artery; AAE ⫽ artery-to-artery embolism; ACA ⫽ anterior cerebral artery; AIF ⫽ anterior
internal frontal artery; CM ⫽ callosomarginal artery; DWI ⫽ diffusion-weighted imaging; FP ⫽ frontal pole; FrP ⫽ frontopolar
artery; GR ⫽ gyrus rectus; ICA ⫽ internal carotid artery; ITO ⫽ in situ thrombotic occlusion; LBO ⫽ local branch occlusion;
MIF ⫽ middle internal frontal artery; MRA ⫽ MR angiogram; Orf ⫽ orbitofrontal artery; PC ⫽ precuneus; PCA ⫽ paracentral
artery; PIF ⫽ posterior internal frontal artery; PL ⫽ paracentral lobule; SFG ⫽ superior frontal gyrus; SMA ⫽ supplementary
motor area; SP ⫽ superior parietal artery; TE ⫽ echo time; TOAST ⫽ Trial of Org 10172 in Acute Stroke Treatment; TR ⫽
repetition time.
Anterior cerebral artery (ACA) territory infarction was first described in the early 20th
century based on autopsy results.1,2 Since then, several CT3-6 or MRI7,8 based studies
investigated etiologies and clinical features. However, the number of patients was gener-
ally too small to make a clinical–MRI correlation, and stroke mechanisms have not been
elucidated in detail, especially in those with intrinsic ACA atherosclerosis.6 The purpose
of the present study was to investigate the etiologic, clinical, and imaging findings in
ACA infarction using MRI and angiographic results. In particular, we wished to eluci-
date detailed stroke mechanisms in patients with intracranial ACA atherosclerosis.
From the Stroke Center and Department of Neurology, University of Ulsan, Asan Medical Center, Seoul, Korea.
Supported by a grant from Brain Research Center of the 21st Century Frontier Research Program funded by the Ministry of Science and
Technology of Korea (M103KV010010 06K2201 01010).
Disclosure: The authors report no disclosures.
Copyright © 2008 by AAN Enterprises, Inc.
METHODS Between January 1996 and May 2007, we had
examined 110 consecutive patients with ACA territory in-
farction (1.1% of total patients with ischemic stroke) who
were admitted to the Asan Medical Center within 1 week
after stroke onset. Excluded were patients with 1) concomi-
tant infarcts in other vascular territories, 2) vasospasm sec-
ondary to subarachnoid hemorrhage, and 3) strictly
subcortical infarction, partly because the number of patients
was small (n ⫽ 2) and partly because of the uncertainty of
the vascular territory due to individual variability. In this
clinical-imaging correlation study, 10 patients were further
excluded because 1) three underwent CT scan only, 2) four
had significant residual neurologic deficits due to previous
strokes, and 3) three did not undergo vascular assessment.
Thus, 100 patients who underwent both MRI and angio-
graphic studies became the subject of our study.
All patients underwent blood tests, urine analysis, chest
X-ray, and 12-lead electrocardiogram. Transthoracic and
transesophageal echocardiography and 24-hour electrocar-
diogram monitoring were performed in selected patients.
MRI was performed with a 1.5 Tesla MR imaging unit (Sig-
na; GE Medical Systems, Milwaukee, WI) with echoplanar
capabilities. The common MRI parameters for diffusion-
weighted imaging (DWI) (repetition time [TR] of 7,500
msec, echo time [TE] of 84 msec, matrix number of 128 ⫻
128, and two b values of 0 and 1,000 s/mm2) and T2-
weighted imaging (TR of 4,500 msec, TE of 118 msec) were
slice thickness of 5 mm, interslice gap of 2 mm, 20 axial
slices, and field of view of 250 mm. Common MR angiogram
(MRA) parameters included flip angle of 20°, matrix number
of 512 ⫻ 512, and field of view of 250 mm. Three-
dimensional TOF MRA of circle of Willis was performed
with TR of 25 msec and TE of 2 msec. Three-dimensional
contrast-enhanced MRA from the aortic arch to the level of
the central skull base was obtained using IV bolus injection
of 20 mL (3– 4 mL/second) of gadopentetate dimeglumine
(Magnevist; Schering, Berlin, Germany) with TR of 6 msec
and TE of 1 msec.
Presumed etiologies were defined as follows: 1) large ar-
tery atherosclerosis, further divided into a) internal carotid
artery (ICA) disease: the patients have significant (⬎50%)
narrowing or occlusion of ipsilateral ICA but without signif-
icant ipsilateral ACA atherosclerosis or emboligenic heart
disease, and b) ACA disease: ipsilateral ACA stenosis/occlu-
sion without significant ipsilateral ICA disease or emboli-
genic heart disease; 2) cardiogenic embolism: there should be
an emboligenic heart disease based on Trial of Org 10172 in
Acute Stroke Treatment (TOAST) stroke classification crite-
ria9 without atherosclerotic diseases in the ipsilateral ICA or
ACA; 3) two or more causes: patients with two or more po-
tential causes of stroke such as those with ICA disease and
emboligenic heart disease; 4) undetermined etiology: The
cause of a stroke cannot be determined after thorough evalu-
ation.
Vascular territories and topographic localization were
determined according to the previous anatomic studies (fig-
ure 1).10-12 ACA territory includes the rostrum, genu, trunk,
and splenium of the corpus callosum, cingulate gyrus, fron-
tal pole/gyrus rectus (frontopolar and orbitofrontal artery
territory), medial aspect of superior frontal gyrus (anterior
and middle internal frontal artery territory), supplementary
motor area (SMA) (posterior internal frontal artery terri-
tory), paracentral lobule (paracentral artery territory), and
precuneus (superior parietal artery territory). Clinical results
Figure 1 Schematic illustration of anterior
cerebral artery territory and artery
branches
Orf ⫽ orbitofrontal artery; FrP ⫽ frontopolar artery; AIF ⫽
anterior internal frontal artery; MIF ⫽ middle internal frontal
artery; PIF ⫽ posterior internal frontal artery; CM ⫽ calloso-
marginal artery; PCA ⫽ paracentral artery; SP ⫽ superior pa-
rietal artery; GR ⫽ gyrus rectus; FP ⫽ frontal pole; SFG ⫽
superior frontal gyrus; SMA ⫽ supplementary motor area;
PL ⫽ paracentral lobule; PC ⫽ precuneus.
were obtained from chart review. Muscle strength was
graded as I to V using the Medical Research Council scale,
and motor dysfunction was considered severe when the
grade of the weakest muscle was ⱕ III. Because the corpus
callosum and adjacent cingulate gyrus are supplied by the
pericallosal artery branches and were usually involved si-
multaneously, we lumped these together in clinical-imaging
correlation study. The SMA, paracentral lobule, and precu-
neus were also lumped together for the same reason. The
imaging analysis was done by one of the authors (S.Y.K.),
blinded to the clinical and angiographic findings. The angio-
graphic result was assessed by a neuroradiologist who was
blinded to clinical findings and a stroke neurologist (J.S.K.).
We defined the result as abnormal only when both agreed.
For statistical analyses, Student t test was used for nu-
merical variables and ␹2 tests for categorical variables.
Fisher exact test was used when the number of cells was
small. All statistical tests were performed with the use of the
SPSS program (version 10.0) and p values ⬍0.05 were re-
garded as indicating significance.
RESULTS Demography and clinical-imaging corre-
lation. There were 58 men and 42 women, ages
ranging from 29 to 88 (mean 65.1) years. Risk fac-
tors as defined previously13 included hypertension
in 70, diabetes mellitus in 38, hypercholesterol-
emia in 37, cigarette smoking in 38, a previous
history of stroke in 24, and a history of coronary
heart disease in 11 patients.
MRI showed 55 left infarcts, 36 right infarcts,
and 9 bilateral infarcts. The corpus callosum/
cingulate gyrus was involved in 68 patients (cor-
pus callosum in 63, cingulate gyrus in 28). In the
corpus callosum, the genu was the most fre-
quently involved (n ⫽ 54), followed by trunk (n ⫽
32), rostrum (n ⫽ 10), and the splenium (n ⫽ 8).
The SMA/paracentral lobule was involved in 55,
Neurology 70 June 10, 2008 (Part 2 of 2) 2387
 Table 1 Clinical symptoms and correlated anatomic location
Symptoms Prevalence
Motor dysfunction 91
Severe motor 43
dysfunction
Hypobulia/apathy/ 43
indifference
Urinary incontinence 30
Grasp reflex 25
Aphasia 18
Sensory deficit† 20
*Expressed as prevalence of symptom in patients with involvement of the region vs prevalence of symptom in patients with-
out.
†Tested in 81 patients.
the superior frontal gyrus in 41, frontal pole/gyrus
rectus in 16, and the subcortical area (caudate
head/anterior putamen/internal capsule) was in-
volved in 6 patients. Whole ACA territory in-
volvement was rare, occurring in only in four
patients.
The prevalence of symptoms and correlated
anatomic location are summarized in table 1. Mo-
tor dysfunction (n ⫽ 91) was the most common
symptom: hemiparesis in 70, leg monoparesis in
18, and paraparesis in 3 patients. In patients with
hemiparesis, the weakness was more severe in the
leg than in the arm in 37 patients. Thus, among
the 91 patients with motor dysfunction, leg weak-
ness was dominant in 58 patients (64%). In 29
patients, the degree of motor dysfunction was
similar between arm and leg, while in four, arm
was weaker than the leg. In these 33 patients, the
shoulder was discrepantly weaker than the hand
in the majority (n ⫽ 25). The motor dysfunction
was severe in 43, and the severe motor dysfunc-
tion was closely related to the involvement of
SMA/paracentral lobule.
Sensory examination was reliably performed
in 81 patients while it was not in others due to
significant abulia or aphasia. Among them, 20 pa-
tients (25%) had dysfunction: hemihypesthesia in
12 patients, sensory symptoms in the leg only in 7,
in the arm only in 1 patient. The sensory dysfunc-
tion was always detected in the paretic limbs. Hy-
pobulia/apathy/indifference shown in 43 patients
2388 Neurology 70 June 10, 2008 (Part 2 of 2)
Correlated lesion location
(no. of patients) Comments
SMA/paracentral lobule (30 of 56,
53.6%, vs 13 of 44, 29.5%,
p ⫽ 0.016)*
Frontal pole/gyrus rectus (13 of Bilateral lesion most
16 patients, 81.3%, vs 30 of 84, common followed by left
35.7%, p ⫽ 0.002) and then right lesions
Corpus callosum/cingulate gyrus
(36 of 68, 52.9%, vs
7 of 32, 21.9%, p ⫽ 0.003)
Superior frontal lobe (25 of 41,
61%, vs 13 of 53,
24.5%, p ⫽ 0.000)
None
Corpus callosum/cingulate gyrus More common in women
(21 of 68, 30.9%, vs than in men
4 of 32, 12.5%, p ⫽ 0.052)
Left lesions in 16, bilateral Global in 8, transcortical in 8,
lesions in 2 patients motor in 2
Always with motor dysfunction
was closely related to involvement of frontal pole/
gyrus rectus, corpus callosum/cingulate gyrus,
and the superior frontal lobe, and occurred most
frequently in patients with bilateral lesions (6 of
9, 66.7%), followed by left sided lesions (28 of 55,
50.9%) and right sided lesions (9 of 36, 25%) (p ⫽
0.016). Hypobulia was closely related to grasp re-
flex (p ⫽ 0.001).
Urinary incontinence, observed in 30 patients,
was not related to particular lesion location.
Aphasia was present in 18 patients (transcortical
mixed aphasia 8, global aphasia 8, motor aphasia
2). Global aphasia was closely related to superior
frontal gyrus involvement (p ⫽ 0.039) while
transcortical aphasia was not related to any par-
ticular lesion location. Grasp reflex (n ⫽ 25) was
more often observed in women (15 of 42, 35.7%)
than in men (10 of 58, 17.2%) (p ⫽ 0.035), and
closely related to corpus callosum/cingulate gyrus
involvement. Alien hand sign was observed in 10
patients. Although patients with involvement of
the corpus callosum/cingulate gyrus more often
had this symptom (9 of 68, 13.2%) as compared
to those without (1 of 32 patients, 3.1%), the dif-
ference was not significant (p ⫽ 0.162). Being
women was marginally related to this symptom
(p ⫽ 0.09).
Other miscellaneous symptoms included emo-
tional lability/incontinence14 (n ⫽ 10), drowsiness/
somnolence (n ⫽ 8),5 acute confusion/agitation (n ⫽
8), motor perseveration (n ⫽ 8), ideomotor apraxia

Table 2 Etiologies of anterior cerebral infarction
No. of patients
Etiologies (n ⫽ 100)
Large artery atherosclerosis 73
ACA disease 61
Branch occlusion 20
Artery-to-artery embolism 12
In situ thromboocclusion 20
Combined 9 tion due to a heart disease. Fifteen patients were
ICA disease (ICA to ACA embolism) 6 considered to have unknown mechanism.
Either ACA or ICA disease 6
Cardiogenic embolism 10
Two or more causes
ICA atherosclerosis ⫹ cardiac 1
embolism
ACA atherosclerosis ⫹ 1 was localized to the area adjacent to the athero-
cardiac embolism
Unknown 15
ACA ⫽ anterior cerebral artery; ICA ⫽ internal carotid ar-
tery.
(n ⫽ 7),5 amnesia (n ⫽ 6), altered consciousness (n
⫽ 4), gaze deviation (n ⫽ 3), parkinsonian features
(bradykinesia, cogwheel rigidity with or without
tremor)15,16 (n ⫽ 3), and anosognosia (unawareness
of the paralytic limbs) (n ⫽ 2 ).
Angiographic findings and presumed stroke mecha-
nisms. Angiographies performed were as follows:
MRA in 77, conventional angiography in 20, and
CT angiography in 12 patients. Seven underwent
both MRA and conventional angiography and
two underwent MRA and CT angiography. Local
ACA atherosclerosis (40 stenoses and 28 occlu-
sion) ipsilateral to the infarct was observed in 68
patients, most frequently at A2 (n ⫽ 38) followed
by A1 (n ⫽ 22), A2–A3 junction (n ⫽ 5), and
A1–A2 junction (n ⫽ 3). For statistics, A1–A2
junction was included in A1 disease (A1 group,
n ⫽ 25) and A2–A3 junction disease in A2 disease
(A2 group, n ⫽ 43). A1 group patients more often
had occlusion (16 of 25, 64%) than A2 group (12
of 43, 27.9%) (p ⫽ 0.001).
General stroke mechanisms. Presumed stroke
mechanisms are summarized in table 2. Among
the 68 patients with ACA disease, 6 had addi-
tional significant ipsilateral ICA disease, and 1
had emboligenic heart disease. Therefore, 61 pa-
tients had infarction caused by intrinsic ACA dis-
ease. Significant ipsilateral ICA disease was
shown in 13 patients (5 occlusion, 8 stenosis),
among whom 6 had concomitant ACA disease
and 1 had emboligenic heart disease. Thus, 6 pa-
tients were considered to have ICA to ACA em-
bolic infarction; 1 had a siphon stenosis while
others had proximal ICA disease.
Emboligenic heart diseases were found in 12
patients: atrial fibrillation in 8, valvular heart dis-
ease in 1, atrial fibrillation and valvular disease in
1, cardiomyopathy in 1, and patent foramen ovale
with right to left shunt in 1 patient. Because two
of them had concomitant, significant atheroscle-
rosis, 10 were considered to have embolic infarc-
Stroke mechanisms in ACA atherosclerosis. After an-
alyzing MRI and angiographic data, we eluci-
dated the following stroke mechanisms in 61
patients with intrinsic ACA disease.
Local branch occlusion (LBO) (n ⫽ 20). The infarct
sclerotic vessel, presumably due to an occlusion
of the orifice of one or more of the perforators
supplying adjacent structures by the local throm-
bus formation.17-19 The infarct was usually limited
to the anterior part of the corpus callosum or the
cingulate gyrus (figure 2A). Occlusion of the fron-
topolar or anterior inferior frontal branch, which
usually stems from A2,10 may produce extension
of the lesion to the anterior part of the superior
frontal gyrus (figure 2, B and C).
In situ thrombotic occlusion (ITO) (n ⫽ 20). The in-
farct extensively involved the whole or the most
part of the ACA territory (figure 2, D and E). It
can be explained by occlusion of the main ACA
trunk. However, a part of cortical areas may be
spared due to collateralization from the MCA or
contralateral ACA.
Artery-to-artery embolism (AAE) (n ⫽ 12). The in-
farcts were usually small, sometimes scattered,
and situated at the areas supplied by distal corti-
cal branches. The infarcts, which can be ex-
plained by artery-to-artery embolism, are often
scattered in the ACA and MCA borderzone area
(figure 3A).
Combination of LBO and AAE (n ⫽ 9). There were
infarcts located adjacent to the atherosclerotic
vessel as in LBO. In addition, scattered infarcts in
the remote area were observed as in AAE (figure
3, B and C). Unlike infarcts caused by ITO, the
lesions were not in continuity with each other.
We then compared patients with intrinsic ACA
atherosclerosis (n ⫽ 61) and those with embolism
from either the heart or ICA disease (n ⫽ 16). The
former group more often had corpus callosal in-
volvement (p ⫽ 0.016) and tended to have hypobu-
lia more often (p ⫽ 0.077) than the latter group.
Stroke mechanisms in patients with bilateral ACA in-
farction. We identified nine patients with bilateral
Neurology 70 June 10, 2008 (Part 2 of 2) 2389
 Figure 2 Examples of stroke caused by local branch occlusion (A–C) and in situ thrombotic occlusion (D, E)

(A) T2-weighted MRI shows an infarct localized to the right anterior portion of the corpus callosum (left figure, small arrows),
which was caused by left anterior cerebral artery stenosis (right figure, large arrow). (B) Upper row: gadolinium-enhanced
T1-weighted MRI shows that the lesions involve the anterior part of the corpus callosum and cingulate gyrus. In addition, a
sagittal image shows involvement of anterior part of superior frontal cortex (black arrows). Lower row: MR angiogram shows
stenosis in the A2 and A3 portion of anterior cerebral artery (white arrows). (C) The diagram schematically illustrates the
occlusion of local branches supplying the corpus callosum due to atherothrombosis in the anterior cerebral artery. Dark area
⫽ thrombosis; gray area ⫽ infracted area. (D) Upper row: T2-weighted MRI shows a large infarct involving whole anterior
cerebral artery territory including the corpus callosum, frontal pole, cingulate gyrus, superior frontal lobe, supplementary
motor area, paracentral lobule, and precuneus. Lower row: MR angiogram shows occlusion of left anterior cerebral artery
(arrow). There was an absent right A1, and right anterior cerebral artery is supplied by a branch from the left A1. (E) The
diagram schematically illustrates extensive thrombotic occlusion of anterior cerebral artery producing whole territory infarc-
tion. Dark area ⫽ thrombosis; gray area ⫽ infracted area.

2390 Neurology 70 June 10, 2008 (Part 2 of 2)


Figure 3 Examples of stroke caused by artery-to-artery embolism (A) or
combined mechanism of local branch occlusion and artery-to-artery
embolism (B)
Left image: diffusion-weighted MRI shows scattered infarcts in anterior cerebral artery–
middle cerebral artery borderzone area. Right image: MR angiogram shows significant steno-
sis in the A2–A3 junction of left anterior cerebral artery. (B) Upper row: diffusion-weighted
MRI shows infarcts at the left anterior corpus callosum and scattered infarcts at distal areas.
Lower row: CT angiogram shows severe stenosis in the A2 portion of left anterior cerebral
artery (arrow). (C) The diagram schematically illustrates the stroke mechanism of combined
local branch occlusion and artery-to-artery embolism. Dark area ⫽ thrombosis; gray area ⫽
infracted area; dots ⫽ emboli.
infarcts; in four, the infarcts were considered to
be caused by proximal ACA disease. In three of
them, the mechanism was AAE; one had occlu-
sion of both ACAs (right A2 and left A1–2 junc-
tion), while another had both A1 occlusion. In
these two, AAE may have occurred from both
ACA diseases. The third had left A1 stenosis, in
whom the emboli may have traveled to the oppo-
site hemisphere through the intact anterior com-
municating artery (A-com). The fourth had left
azygos ACA supplying both hemispheres with the
absent right A1. The stroke mechanism was con-
sidered combined (LBO⫹AAE). In three patients,
the mechanism was an embolism either from ICA
or ACA. One patient had left ICA occlusion and
left A1 occlusion. Another had unilateral ICA ste-
nosis and bilateral A2 stenosis. The third had left
ICA occlusion and left A1 occlusion with the ab-
sence of right A1. One patient had emboligenic
heart disease, in whom the emboli probably trav-
eled to bilateral ACAs. Finally, the mechanism
was unknown in one patient.
DISCUSSION Although the prevalence of ACA
infarction in our series was similar to previous
results,4-7 the stroke mechanisms were different.
Studies from western countries showed that ACA
infarction is usually caused by embolism,4,5 while
a Japanese study reported that ACA atherosclero-
sis was the most important etiology.6 Our study
with a much larger number of patients confirmed
that intrinsic ACA disease is the most common
etiology in the East Asian region.
The difference reflects ethnic differences in the
location of cerebral atherosclerosis,20-22 but also
implies that the incidence of ACA atherosclerosis
could have been underestimated in previous stud-
ies where vascular imaging was incompletely per-
formed. The relative rarity of embolism in ACA
infarction as compared to MCA territory infarc-
tion19 may be related to the fact that the diameter
of A1 is only about half of the MCA and that
communications between both ACAs through the
A-com10 might play a role in the clearance of em-
boli.
We proposed novel stroke mechanisms in pa-
tients with intrinsic ACA diseases: LBO, AAE,
and ITO. LBO represents occlusion of an orifice
of smaller branches arising from the proximal
ACA due to local thrombosis.17-19,23 Because ath-
erosclerotic changes occurred most frequently at
A2 segment followed by A1, and A2–A3 junction,
perforators as well as orbitofrontal, frontopolar,
or anterior internal frontal arteries arising from
these segments10 can be occluded, resulting in in-
farcts usually restricted to the anterior part of the
corpus callosum, cingulate gyrus, and adjacent
frontal areas (figure 2, A and B). We also ob-
served patients with AAE and those with a com-
bined mechanism of LBO and AAE. Thus, the
stroke mechanisms seem to be similar to that of
intrinsic MCA atherosclerosis,18,19 except that
ITO producing a large infarct is more prevalent in
ACA infarction. However, even in patients with
ITO, the cortical area was often spared, probably
due to collateralization from the MCA or con-
tralateral ACA. The embolic infarcts related to
AAE were often scattered at the ACA and MCA
borderzone area (figure 3), which may be ex-
plained by the insufficient washing out of emboli
Neurology 70 June 10, 2008 (Part 2 of 2) 2391
 in the hypoperfused area18,24 in the presence of se-
vere ACA stenosis. Therefore, aside from stroke
mechanisms so far described, the status of collat-
eral circulations and hemodynamic factors ap-
pear to play additional roles in determining the
pattern of ACA infarction and consequent clinical
syndromes. We also found that mechanisms for
bilateral infarcts included embolism from the ICA
or the heart traveling to both hemispheres, simul-
taneous embolization from both ACA stenoses,
and emboli from the A1 stenosis traveling to both
hemispheres through the A-com.
As expected, severe motor dysfunction was
closely associated with SMA/paracentral lobule
involvement. Although predominant leg weak-
ness was usual, identical weakness between arm
and leg was not uncommon. Because the shoulder
was discrepantly weaker than the hand in the ma-
jority of these patients, a partial involvement of
arm-presenting motor fibers2,5,25 seems to explain
the arm weakness, although the possible presence
of motor neglect26,27 cannot be ruled out.
Our data showed that callosal or anteromedial
frontal damages are responsible for hypobulia/
apathy/indifference, which was consistent with
previous observations.28,29 These symptoms are
more prevalent in patients with bilateral lesions
followed by those with left lesions. Although uri-
nary incontinence was considered to be related to
lesions affecting the superior frontal gyrus, cingu-
late, and the white matter in between,25,30 we
failed to find any specific anatomic location re-
lated to this symptom, as in previous studies.5,31,32
Perhaps urinary incontinence may be related to
extensive lesions involving multiple neuronal
pathways regulating bladder function.
We found that transcortical aphasia character-
istically occurred in patients with ACA infarc-
tion.5,25,33,34, However, we also observed as many
patients with global aphasia. The aphasia might
be a manifestation of abulia. However, we con-
sidered that the speech dysfunction of these pa-
tients was out of proportion of the abulia.
Moreover, out of 16 patients with aphasia, 6 did
not have abulia. Unlike the patients with MCA
infarction, the aphasias tended to improve rap-
idly. Thus, we assumed that the initiation or reg-
ulation of speech may be dysfunctional in patients
with medial frontal lesions,12,33,35,36 which could
result in transient aphasia. Our finding that
global aphasia was closely related to medial supe-
rior frontal lobe involvement seems to be consis-
tent with this theory. Grasp reflex was closely
related to corpus callosum/cingulate involvement.
This and alien hand phenomenon tended to occur
2392 Neurology 70 June 10, 2008 (Part 2 of 2)
more frequently in women than in men, which
may be consistent with the previous notion that
connecting fibers in the corpus callosum are more
abundant in women than in men.37
There are limitations in our studies. First, this
is a retrospective study, and inaccurate or insuffi-
cient assessment might have been present. Sec-
ond, because the patients were recruited from a
tertiary hospital, they may not represent the gen-
eral stroke population. To minimize referral bias,
we selected patients who were admitted within 1
week after onset. Third, MRA was usually used
in this study, which is not sensitive enough in the
evaluation of distal arteries. Thus, at least some
of the patients classified as having unknown
mechanism may have arterial diseases at distal
branches. Finally, all our patients were Korean,
and our data may not be generalizable to other
ethnic groups.
Received September 28, 2007. Accepted in final form Febru-
ary 20, 2008.
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