From the Departments of Neurology (J.S.K., J.H.L.) and Radiology
(C.G.C.), University of Ulsan, Asan Medical Center, Seoul, South Korea.
Correspondence to Jong S. Kim, MD, Department of Neurology, Asan Medical Center, Song-Pa PO Box 145, Seoul 138–600, South Korea. E-mail jongskim{at}www.amc.seoul.kr
Methods—The subjects included 34 patients with LMI who underwent
both MRI and conventional angiography. We analyzed the risk
factors, clinical features, MRI findings, and angiography results. The
size of the infarction was also measured. We attempted to correlate the
MRI findings with the vascular lesions shown in the angiograms.
Results—Presumed causes for infarction were atherothrombosis in
19 patients, arterial dissection in 8, cardiogenic embolism
in 3, moyamoya disease in 1, small-vessel disease in 1, and
embolism of unknown source in 2. Isolated posterior
inferior cerebellar artery (PICA) disease (n=8) was usually
associated with atherothrombosis and correlated with thin, round, or
diagonal band–shaped lesions in the lateral-superficial area of the
caudal medulla and/or dorsolateral portion of the rostral-middle
medulla. Short-segment distal vertebral artery (VA) disease (n=9) was
usually due to atherothrombosis and correlated with small lateral
caudal and/or medium-sized, diagonal band–shaped rostral-middle
medullary lesions. There were 13 patients with long-segment VA disease
sparing (n=8) or involving (n=5) the proximal part of the VA with
concomitant occlusion of the PICA in 7 patients. This vascular lesion
produced either large MRI lesions extending ventrally (n=5; 4 were
associated with VA dissection) or small lesions mimicking those
produced by isolated PICA disease (n=8; 6 were associated with
atherothrombosis and 1 patient had moyamoya disease). These large
MRI lesions characteristically produced bilateral or contralateral
trigeminal sensory involvement. Normal angiogram (n=4; 3 patients were
presumed to have cardiac embolism, one lesion was associated with
small-vessel infarction) was associated with small, round lesions that
produced minor and fragmentary symptoms. Among these subgroups, the
size of the infarct in the patients with long-segment VA disease due to
dissection was significantly larger than that of the patients with
other vascular lesions.
Conclusions—Our data suggest that the heterogeneous
MRI lesions (and consequent clinical syndromes) of LMI are correlated
with diverse angiographic findings, which in turn are due to different
pathogenic mechanisms: etiology, location and size of the involved
vessels, speed of the lesion development, and status of collateral
channels. Generally, infarcts related to multiple vessel involvement,
dissection, and poor collateral circulation are larger than those
associated with single-vessel disease, long-standing
atherothrombosis/cardiac embolism, and good collateralization.
Because no patients showed findings of a fusiform aneurysm or a
double lumen sign characteristic of vertebral dissection in angiogram
or in the axial cross-sectional MRI images,7 8 we
arbitrarily defined the etiopathogenesis as follows.
Probable dissection was defined as (1) obvious history of recent
(within 1 week) head/neck trauma or sudden neck rotation (chiropractic
manipulation, golf practice, yoga, etc), (2) concurrent severe neck or
occipital pain, (3) no evidence of atherosclerotic vascular changes on
angiogram, and (4) angiographic findings of an elongated, usually
tapered stenosis/occlusion in the involved
artery9 10 ; possible dissection was defined as
above except that there was no definite history of recent head/neck
trauma/rotation.
Atherosclerosis (or atherothrombosis) was defined as
present in patients (1) with at least one conventional risk factor
for atherosclerosis, (2) with angiographic evidence of
atherosclerotic vascular lesion, and (3) who do not fit the category of
dissection.
Probable cardiogenic embolism was defined as the presence of concurrent
emboligenic heart disease (atrial fibrillation, prosthetic
valve, sick sinus syndrome, valvular disease,
cardiomyopathy, recent myocardial infarction)
without risk factors for atherothrombosis; possible embolism was
defined as patent foramen ovale with right to left shunt without risk
factors for atherothrombosis.
Small-vessel disease was defined as (1) presence of hypertension, (2)
age >50 years, (3) no emboligenic heart disease, and (4) normal
angiogram.
The patients' MRI findings were copied from the original film
(T2-weighted axial image) by one of the authors (J.S.K.) who was
blinded to the angiogram findings. According to the previous
criteria,4 the level of medulla shown in MRI was
categorized as rostral, middle, and caudal. The size (area) of an
infarct was measured with the Leica Q-500 MC image analyzer
(Cambridge Ltd) and was presented as the cross-sectional area
of infarction/whole medullary area at that segment x100 (%). When
there were two cuts of MRI demonstrating the lesion, the larger lesion
was used for the analysis. All data regarding the average size
of the infarction were expressed as mean±SD. Comparison of the size of
the lesion among different subgroups (see below) was done by
Wilcoxon rank sum tests, with the use of the SAS statistical
package (version 6.0). Angiography results were schematically drawn by
another author (J.H.L.) who was blinded to the MRI findings. They were
also reviewed by a neuroradiologist (C.G.C.) who was unaware of the MRI
findings.
The patients' major neurological symptoms/signs were vertigo/dizziness
(88%), gait ataxia (88%), Horner's sign (88%), nystagmus (71%),
nausea/vomiting (65%), dysphagia (62%), and hoarseness (41%).
Sensory manifestations included crossed pattern (ipsilateral
trigeminal–contralateral hemibody/limb) in 11, contralateral
trigeminal pattern in 10, bilateral trigeminal pattern in 4, each of
which probably was due to an involvement of the descending trigeminal
tract, the ascending secondary trigeminal tract, and both tracts,
respectively.4 Isolated hemibody/limb sensory
involvement and isolated trigeminal sensory changes were noted in 6 and
2 patients, respectively. One patient did not show any sensory
abnormalities.
Angiographic Findings and MRI-Angiogram Correlation
Isolated PICA Disease
MRI Findings
Clinical Manifestations
Presumed Pathogenesis
Short-Segment VA Stenosis
MRI Findings
Clinical Manifestations
Presumed Pathogenesis
Long-Segment VA Disease Sparing the Proximal Portion
MRI Findings
Clinical Manifestations
Presumed Pathogenesis
Long-Segment VA Occlusion Including the Proximal Portion
MRI Findings
Clinical Manifestations
Presumed Pathogenesis
Normal Angiographic Findings
MRI Findings
Clinical Manifestations
Presumed Pathogenesis
Size of Infarct in Each Subgroup
In this study, angiography demonstrated isolated PICA disease in 23.5%
of patients, VA disease in 38.2%, involvement of both VA and PICA in
26.5%, and normal results in 11.8%. Previously, Fisher et
al11 reviewed the pathological findings of 42
patients with LMI (26 from the literature and 16 of their own) and
found that PICA disease, VA disease, and involvement of both arteries
were seen in 14.3%, 38.1%, and 26.2%, respectively. In 19% of these
patients, occluded vessels were not found. Thus, our results were
similar to those of Fisher et al, except that isolated PICA disease was
more frequent and normal findings were less frequent. This may be
attributed to selection bias; conventional angiography was likely to
have been performed in patients who were expected to have a gross
vascular lesion. This selection bias may also explain, at least in
part, the younger average age of the patients (50 years) compared with
patients with stroke in general in our hospital (62 years), as well as
the relatively frequent arterial dissection in our series
(24%) compared with the previous study (14% in the series of
Vuilleumier et al6 ). Thus, the prevalence of each
of the pathogenetic mechanisms for LMI shown in our study may not be
generalizable.
We found that isolated PICA disease was associated with relatively
small, thin lesions in the lateral caudal and/or dorsolateral
middle-rostral portion of the medulla. The lesion was located at
various rostral-caudal levels of the medulla, which may result from
various levels of PICA origin at the VA,11
various lengths of the ascending loop of PICA,12
different degree of collateralization from other vessels such as the VA
or the AICA,11 and different levels of the
occlusion of penetrating branches from the PICA (Fig 10
In our study, VA stenosis or occlusion was the most common
angiographic feature. Short-segment VA stenosis tended to
produce a medium-sized, diagonal band–shaped lesion usually confined
to the dorsolateral part of the rostral-middle medulla or lateral
superficial portion of the caudal medulla. It seems that the level of
stenosis at the VA determines the rostrocaudal level of the MRI
lesion. The lesion usually produced classic lateral medullary syndrome
with a crossed sensory pattern. The MRI lesion of short-segment VA
disease does not appear to be distinctly different from that produced
by PICA disease in its morphology and size, suggesting that territories
supplied by branches from the PICA and VA frequently overlap (Fig 10
Long-segment VA diseases were divided into those with sparing of the
proximal part of the VA and those without. According to the
MRI–vascular lesion correlation, however, it seems more reasonable to
divide VA disease into that producing a large MRI lesion and that
associated with a small lesion. The long-segment VA disease associated
with a large lesion involving the whole dorsolateral-ventromedial part
of the medulla was most often caused by dissection. The large lesion
was probably caused by simultaneous occlusion of multiple
branches of the VA with or without PICA involvement (Fig 10
Finally, patients with normal angiogram frequently had a cardiac source
of embolism, and the embolic occlusion appears to have been recanalized
at the time of angiography. The successful
recanalization may have resulted in a small infarct
restricted to the most vulnerable area, producing fragmentary symptoms
in this group. Small dorsal lesions affecting a limited area produced
isolated facial sensory changes in patients 32 and 33 by selective
involvement of the descending trigeminal tract/nuclei (Fig 8
In summary, our study illustrates that LMI is a
heterogeneous condition associated with various MRI lesions
and diverse vascular pathologies. Isolated PICA disease usually
produces thin lesions at various rostrocaudal levels leading to mild
symptoms, and short-segment VA disease is associated with classic
diagonal band–shaped lesions confined to the lateral-posterior medulla
leading to classic symptom complexes. Both are associated with
atherothrombotic vascular disease. Long-segment VA disease is
associated with either large MRI lesions or lesions mimicking isolated
PICA disease that are most often related to dissection and
atherothrombosis, respectively. Patients with normal angiogram often
had emboligenic cardiac disease and had relatively small lesions
producing fragmentary symptoms. These principles may be much too
simplified to account for the complexity of LMI and are indeed open to
further verification through analysis of more cases.
Received November 24, 1997;
revision received January 5, 1998;
accepted January 5, 1998.
© 1998 American Heart Association, Inc.
Original Contributions
Patterns of Lateral Medullary Infarction
Vascular Lesion–Magnetic Resonance Imaging Correlation of 34 Cases
Abstract
Top
Abstract
Introduction
Subjects and Methods
Results
Discussion
References
Background and Purpose—Correlation
of MRI findings with various vascular pathologies has rarely been
attempted in patients with lateral medullary infarction (LMI). The aim
of the present study was to correlate the diverse MRI lesions with
the vascular lesions seen on conventional cerebral angiography in
LMI.
Key Words: medulla oblongata • cerebral infarction • magnetic resonance imaging • angiography • thrombosis • dissection
Introduction
Top
Abstract
Introduction
Subjects and Methods
Results
Discussion
References
With the advent of
MRI, medullary infarctions are now easily
recognized,1 2 3 4 5 6 and recent
studies4 6 have shown that the MRI-identified
lesions are quite diverse and generally correlate with
heterogeneous clinical syndromes in these patients.
However, whether the diverse MRI lesions have any implication for
different etiopathogeneses has not been studied sufficiently. Although
one recent study6 tried to address this issue,
vascular status was analyzed for the most part with MR
angiography, which according to our experience frequently failed to
provide us with reliable information regarding the status of the PICA.
Therefore, whether etiopathogenetic heterogeneity
correlates with diverse medullary lesions remains to be explored. In
the present study, we describe 34 patients with LMI in whom MRI
showed appropriate lesions, and we attempted to correlate the MRI
findings with the conventional angiography results.
Subjects and Methods
Top
Abstract
Introduction
Subjects and Methods
Results
Discussion
References
At the Asan Medical Center, we examined 64 patients with
clinically suspected LMI between September 1994 and May 1997. Sixty-one
of them underwent MRI; axial T2 (repetition time, 2500 ms; echo time,
80 ms), proton-density, and gadolinium-enhanced T1-weighted scans were
performed in the horizontal plane at 3-mm intervals from the medulla to
the midbrain. A sagittal T1-weighted image was also obtained. Of these
patients, we selected 34 in whom (1) MRI showed an appropriate
medullary lesion and (2) conventional (transfemoral) angiography was
performed. There is no standardized selection criteria for performing
conventional angiography in our hospital, but generally patients who
were elderly, had a poor clinical status, or did not give consent did
not undergo this study. Patients who underwent MR angiography were not
included in the present study because the results of this technique
were considered insufficient in the precise evaluation of the
PICA.6 Risk factors for stroke such as
hypertension, diabetes mellitus, current cigarette smoking, habitual
alcohol drinking (more than 2 times a week or binge drinking), and
heart disease were recorded.
Electrocardiography was performed in all
patients, and those who were <50 years of age or without conventional
vascular risk factors underwent transthoracic and
transesophageal echocardiograms.
Results
Top
Abstract
Introduction
Subjects and Methods
Results
Discussion
References
General Features
The demographic characteristics, risk factors, and clinical
features of 34 patients are summarized in the
Table
. There were 26 men and 8 women aged
from 28 to 73 years (mean, 50 years). The presumed pathogenetic
mechanisms of infarction were atherothrombosis in 19 patients,
arterial dissection in 8 (probable 5, possible 3),
small-vessel disease in 1 (patient 32), and moyamoya disease in 1
(patient 26). Cardiogenic embolism was considered in 3 (probable 1,
possible 2). Although 2 additional patients had patent foramen ovale
with right to left shunt, they were included in the group of
atherothrombosis because they had multiple risk factors and
atherosclerotic changes on angiogram. One (patient 3) had decreased
serum free protein S, and in 1 (patient 14) the etiopathogenesis was
unclear. These 2 patients were considered to have an embolism of
unknown source. Except for 1, all patients with arterial
dissection were younger than 50 years.
View this table:
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Table 1. Clinical Features and Risk Factors of Patients
The patients' MRI findings and angiographic results were combined
and are presented in Figs 2, 4, 6, and 8. The majority of the
patients had distal VA disease (stenosis or occlusion).
Stenosis >50% was considered significant in this study. For
further clarification, the length of the stenotic/occlusive
segment was classified as "short" when the involved area was <2 cm
and "long" when it was longer than 2 cm. In general, there was
isolated PICA stenosis/occlusion in 8 patients (23.5%),
isolated VA disease in 13 (38.2%), and involvement of both VA and PICA
in 9 (26.5%). In 4 patients (11.8%) no angiographic abnormalities
were seen.
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Figure 2. MRI and angiographic findings of patients with
PICA stenosis/occlusion. The size of PICA was exaggerated for
clear viewing. Dotted area indicates stenosis and dark area
indicates occlusion. Number indicates patient number; C, caudal; M,
middle; R, rostral; +med, cerebellar involvement of medial PICA
territory; AS, atherosclerosis; EmbUK, embolism of
unknown source; and Dis>, possible dissection.
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Figure 4. MRI and angiographic findings of patients with
short-segment VA disease without (patients 9 through 14) and with
(patients 15 through 17) PICA occlusion. Dis 
indicates probable
dissection; other abbreviations are defined in Fig 2
.
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Figure 6. MRI and angiographic findings of patients with
long-segment VA disease without (patients 18 through 25) and with
(patients 26 through 30) proximal VA involvement. +S indicates
scattered cerebellar infarction; +, cerebellar infarction with whole
PICA territory; and Dis , probable dissection. Other abbreviations
are defined in Fig 2.
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Figure 8. Patient 32. T2-weighted MRI shows a small infarct
in the right rostral medulla (arrow) that was probably caused by
cardiogenic embolism. Angiogram findings were normal in this
patient.
There were 8 patients with isolated PICA disease (4
stenosis, 4 occlusion; patients 1 through 8, Figs 1 and 2).
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Figure 1. Patient 6. A, T2-weighted MRI shows an infarct in
the right caudal medulla. B, Angiogram shows a focal stenosis
in the proximal portion of the PICA (arrow) caused by possible
dissection.
In this group, the MRI lesion was generally small, thin (except
patient 2), and located at various levels: caudal (n=2), middle (n=3),
rostral (n=1), caudal and middle (n=1), and middle and rostral (n=1)
medulla. It represented a small lesion involving the
lateral caudal (patients 5 and 6)/dorsal middle-rostral (patients 5 and
7) medulla or a diagonal band–shaped lesion involving the
posterolateral medulla (patients 1, 3, and 4). Cerebellar involvement
(medial PICA territory) was seen in only 1 patient (patient 5).
The patients' symptoms were usually mild and often fragmentary.
Sensation in the face was retained in patients 5 through 7, and patient
8 did not have sensory symptoms.
Six patients had atherothrombosis, and 1 had possible dissection.
Patient 6 with possible dissection had a small aneurysm at the
PICA-VA junction area. One did not have a stroke risk factor but had
decreased serum protein S level and was categorized as having an
embolism without obvious source.
Of the 9 patients with short-segment VA
stenosis, there were 3 with and 6 without PICA occlusion
(patients 9 through 17, Figs 3 and 4). The vascular lesion was located below
(n=2) or above (n=3) the PICA origin. In 3 (patients 15 through 17),
the lesion was at the PICA orifice and occluded the PICA. In 1 (patient
14), the PICA was considered to be absent congenitally because it was
unidentifiable in both sides and the AICA was predominantly
supplying the lower part of the cerebellum. In this patient the lesion
appeared to be a small filling defect rather than a stenosis,
suggesting an embolic disease, but we were unable to localize the
embolic source.
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Figure 3. Patient 15. A, T2-weighted MRI shows an
infarct in the left middle-rostral medulla. B, Angiogram shows a focal
stenosis in the left VA (arrow) with nonvisualization of the
PICA, which was probably caused by atherothrombosis. There also was
significant stenosis in the proximal portion of the right
AICA.
The lesions were variously located at the caudal
(n=1), middle (n=1), rostral (n=1), caudal and middle (n=3), and middle
and rostral (n=2) medulla. They were characterized by
lateral-superficial lesions at the caudal medulla (patients 9, 12, and
16) or posterolateral lesions at the middle-rostral medulla. Generally,
the proximal (lower) vascular lesion was correlated with a caudal
medullary lesion (patients 9 and10), and distal vascular
lesions tended to produce rostral lesions (patients 13 and 14; patient
12 was an exception). Cerebellar involvement was not seen in any
patient.
The lesions tended to produce classic lateral medullary syndrome
(for example, 5 patients had a classic crossed sensory pattern).
Six patients had atherothrombosis, 2 had
arterial dissection (1 probable and 1 possible), and 1 had
an embolism of unknown source.
Long-segment VA disease sparing the portion proximal to the C1
segment of the VA was seen in 8 patients (2 stenosis, 6
occlusion; patients 18 through 25, Fig 5
and Fig 6, upper row). In this group, the
long-segment distal VA was involved up to the vertebrobasilar junction
or PICA orifice. In 3 patients (patients 23 through 25), PICA was
occluded by the diseased VA, whereas in others (n=5) the PICA was
spared. Among those patients, 3 (patients 20 through 22) had a high
PICA origin (therefore the vascular lesion was located below the PICA
origin), and 1 (patient 18) had a low PICA origin (the lesion was above
the PICA).
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Figure 5. Patient 20. A, T2-weighted MRI shows an infarct in
the right middle medulla. B, Angiogram shows a long-segment occlusion
in the right VA that was probably caused by dissection.
The lesion was located in the middle medulla in 4 patients, caudal
and middle medulla in 3, and middle and rostral medulla in 1. One
(patient 25) with concomitant PICA involvement had scattered infarcts
in the cerebellum. Five patients (patients 18 through 20, 23, and 24)
had large infarcts encompassing the posterolateral-ventromedial part of
the medulla, whereas in 3 the lesions were relatively small.
This group was characterized by relatively frequent bilateral
trigeminal (n=3) or contralateral trigeminal (n=2) sensory pattern.
However, the 3 patients with small lesions showed a crossed sensory
pattern.
Mechanisms included arterial dissection in 5 patients
(probable dissection in 4, possible dissection in 1) and
atherothrombosis in 3. Two of the 3 patients with atherothrombosis
(patients 22 and 25) had lesions that were relatively small.
Long-segment VA occlusion including the portion proximal to the C1
segment was seen in 5 patients (patients 26 through 30, Fig 7 and Fig 6, lower row). In this group,
the vascular lesions ranged from the origin of the VA to the distal
part of the vessel. In 4 patients, the lesion occluded the PICA,
whereas in 1 the lesion ended just distal to the origin of the
PICA.
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Figure 7. Patient 26. Top, T2-weighted MRI shows an infarct
in the left middle medulla. Bottom, Angiogram shows nonvisualization of
the left VA. Thyrocervical trunk (arrow) is shown with prominent
collaterals (right panel). A part of the upper cervical portion of the
VA (arrowhead) was faintly visualized through collaterals from the deep
cervical branches (arrow), but the distal part of the VA was not
visualized, suggesting occlusion (left panel). This patient had a
bilateral distal internal carotid artery occlusion with rete mirabile
consistent with moyamoya disease.
The lesions were located in the caudal medulla in 3 patients,
caudal and middle medulla in 1, and middle and rostral medulla in 1.
The infarct was generally small in size and variously located:
lateral-superficially (patients 28 and 29) or posterolaterally in a
diagonal-band shape (patients 26 and 30) at the caudal medulla. Lesions
also involved the most dorsal part of the middle-rostral medulla in
patients 27 and 30. Cerebellar involvement was seen in 1 patient (whole
PICA territory).
The patients showed marked gait ataxia and mild dysphagia. The
sensory pattern was heterogeneous.
Pathogenesis included atherothrombosis in 4 patients and
moyamoya disease (complete occlusion of both distal carotid
arteries with typical rete mirabile) in 1 patient (patient 26).
Angiographic findings were normal in 4 patients (Figs 8 and 9).
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Figure 9. MRI findings of patients with normal angiographic
results. CE indicates probable cardiogenic embolism; CE>,
possible cardiogenic embolism; and SVI, small-vessel infarction. Other
abbreviations are defined in Fig 2.
The lesions were small in size, relatively round, and
heterogeneously located. The cerebellum was spared in
all.
There was a paucity of symptoms, and sensory signs were often
fragmentary; 2 patients had ipsilateral sensory changes limited to the
face.
The causes included cardiac embolism in 3 patients (probable 1,
possible 2), and small-vessel infarction in 1 patient.
The average sizes of infarct in patients with PICA disease,
short-segment VA disease, long-segment disease with proximal VA
involvement, and normal angiogram were 14.14±8.95%, 15.78±7.11%,
10.63±6.05%, and 9.19±3.71%, respectively, and were not
significantly different from each other. However, the size of the MRI
lesion in patients with long-segment VA disease sparing the proximal VA
(average size, 27.78±9.28%) was significantly larger than those of
all other groups (P<.05, in all). In the patients with
long-segment VA disease, we also attempted to compare the infarct size
of the patients with dissection (patients 18 through 21 and 23) with
that of the patients with atherosclerosis (patients 22
and 24 through 30). We found that the former was significantly larger
than the latter (P<.05). In patients with short-segment VA
disease, the average infarct size of the patients with concomitant
occlusion of PICA was larger (23.83±2.74%) than in those without
(average, 11.76±9.07%), which, however, was not significantly
different on statistical analysis.
Discussion
Top
Abstract
Introduction
Subjects and Methods
Results
Discussion
References
Although various patterns of MRI lesions and vascular pathologies
have been previously shown to be associated with LMI, how they are
correlated with each other remains unexplored. Ours is the first
attempt to analyze the location, shape, and size of the
MRI-identified lesions with conventional angiographic findings in a
relatively large number of patients. The results provided basic insight
as to how the heterogeneous vascular lesions are related
with the various patterns of infarcts (and consequent clinical
syndromes) occurring in the lateral medulla. ). The most dorsal part of the caudal
medulla was usually spared. This area (supplied by the posterior spinal
artery, a relatively distal branch of the PICA13 )
may easily be spared, probably because atherosclerotic changes are
generally more severe in the proximal than the distal part of the PICA.
Regardless of the explanation, the heterogeneous lesion
location is consistent with heterogeneous clinical
manifestations (such as sensory pattern), but the clinical symptoms
were generally mild, probably because of the thinness of the lesions.
The fact that the dorsal part of the caudal medulla, in which the
descending trigeminal tract/nuclei are located,13
is frequently spared may explain the absence of trigeminal sensory
symptoms in patients 5 through 8. Our data illustrate that PICA
territory is not strictly confined to a certain part of the medulla, as
suggested by previous authors.6 13 Furthermore,
cerebellar involvement was noted in only 1 of 8 patients with isolated
PICA disease, illustrating the effectiveness of the collateral
circulation in the cerebellum through the AICA or the superior
cerebellar artery.12
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Figure 10. Schematic drawing of the vascular lesion (dotted
area) and resultant MRI lesion. ).
Furthermore, although statistical significance was not reached, the
average size of the infarct was larger in patients with concomitant
PICA occlusion than that in those with spared PICA, which may reflect
an involvement of both arteries leading to a relatively large lesion
due to poor collateral circulation. ). The
clinical hallmark of the large MRI lesions was bilateral or
contralateral trigeminal sensory involvement that was caused by
concomitant involvement of the medial-ventrally located ascending
secondary trigeminal fibers.4 On the other hand,
patients with atherothrombotic disease had small MRI lesions despite
extensive vascular disease, which may be attributed to previously
established collateralization in patients with slowly progressive
atherothrombosis or moyamoya disease (Fig 7). The MRI lesion in
these patients was similar in shape and size to that produced by
isolated PICA disease, suggesting that the lateral medulla supplied by
the medial PICA may have poor collateral
circulation.12 Thus, it seems that not only the
length of the involved VA segment but also the speed of development of
the vascular lesion determine the eventual size of the infarct and
consequent clinical syndromes. ).
According to previous authors6 and our own
experiences, patients with cerebellar infarction may exhibit symptoms
of LMI without visible lesion in the medulla. These cases were omitted
in our series because we considered only the patients with
MRI-identified medullary lesions. Thus, the prevalence of cardiogenic
embolism may have been underestimated in our study.
Selected Abbreviations and Acronyms
AICA
=
anterior inferior cerebellar artery
LMI
=
lateral medullary infarction
PICA
=
posterior inferior cerebellar artery
VA
=
vertebral artery
Acknowledgments
We thank S.S. Yoon, RN, and Y.S. Kim for their help in preparing
the manuscript.
References
Top
Abstract
Introduction
Subjects and Methods
Results
Discussion
References
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