1405
Spectrum of Lateral Medullary Syndrome
Correlation Between Clinical Findings and Magnetic
Resonance Imaging in 33 Subjects
Jong S. Kim, MD; Jay H. Lee, MD; Dae C. Suh, MD; Myoung C. Lee, MD
Downloaded from http://stroke.ahajournals.org/ by guest on July 31, 2017
Background and Purpose Computed tomography is insufficient in evaluation of medullary lesions. Although lateral
medullary infarction is a relatively common type of cerebrovascular disease, detailed correlation between clinical findings and magnetic resonance imaging (MRI) has not yet been
reported.
Methods We studied 33 consecutive patients with lateral
medullary infarction who showed appropriate MRI lesions
and correlated their clinical findings with the MRI results.
Results Gait ataxia (88%), vertigo/dizziness (91%), nausea/
vomiting (73%), dysphagia (61%), hoarseness (55%), Horner
sign (73%), and facial (85%) and hemibody (94%) sensory
changes were frequent clinical findings. MRI results showed
that the lesions located in the rostral part of the medulla were
usually diagonal band-shaped and were associated with more
severe dysphagia, hoarseness, and the presence of facial
paresis, whereas the caudal lesions, situated usually in the
lateral surface of the medulla, appeared to correlate with more
marked vertigo, nystagmus, and gait ataxia. Nausea/vomiting
and Horner sign were common regardless of the lesion location, and lesions extending ventromedially correlated with
facial sensory change on the contralateral side of the lesion.
Conclusions Analysis of MRI findings in rostrocaudal and
dorsoventral aspects allows us, although not unequivocally, to
make anatomicoclinical correlations in the evaluation of patients with lateral medullary stroke syndrome. (Stroke. 1994;
25:1405-1410.)
Key Words • cerebral infarction • lateral medullary
syndrome • magnetic resonance imaging • stroke
assessment
C
yond the dorsolateral portion were included. The 33 patients
comprised 22 men and 11 women (age range, 36 to 71 years
[mean, 59 years]). Risk factors for stroke included hypertension in 24, hyperlipidemia in 9, diabetes mellitus in 8, cigarette
smoking in 8, and cardiac disease in 3. No significant risk
factors were identified in 3 patients. All patients except 2 were
examined within 5 days after the onset of stroke. Their main
clinical symptoms and signs were evaluated as follows: vertigo/
dizziness: — (absent), -I- (present); nystagmus: — (absent), +
(present on extreme gaze), + + (present on forward gaze); gait
ataxia: - (absent), + (present but able to walk), + + (unable
to walk); nausea/vomiting: - (absent), + (present); dysphagia:
- (absent), + (mildly present), ++ (needs nasogastric tube
for feeding); hoarseness: - (absent), + (present); Horner
sign: — (absent), + (present); facial palsy: — (absent), +
(present); hemiparesis: - (absent), + (present); and sensory
dysfunction (depicted in Fig 1).
MRI studies were performed using a 1.5-T superconducting
magnet (GE). Axial T2 (repetition time [TR], 2500 milliseconds; echo time [TE], 80 milliseconds) scan was performed in
horizontal plane at 5- or 6-mm intervals from the medulla to
the midbrain. T,-weighted (TR, 600 milliseconds; TE, 20
milliseconds) axial and sagittal images were also obtained.
Coronal sections were done in two cases. Evaluation of the
lesions generally depended on T2-weighted axial cuts of the
medulla, which are imaged at three different levels*: the upper
medulla, characterized by posterolateral bulging of the restiform body (Fig 2, top left panel); the middle medulla, characterized by nodular lateral surface due to the olivary nucleus
(Fig 2, top right panel); and the lower medulla, characterized
by a relatively round figure with closed fourth ventricle (Fig 2,
bottom left panel). The patients' MRI findings were evaluated
in rostrocaudal and dorsoventral aspects.
omputed tomography (CT) usually fails to identify
medullary vascular lesions. With the advent of
magnetic resonance imaging (MRI), brain stem
ischemic strokes can be more definitively evaluated.1-2
Ross et al3 found MRI-identified lesions in their 4 patients
with lateral medullary syndrome (LMS), and Bogousslavsky et al4 described 6 patients who had small vertebrobasilar territory infarcts with good clinical-MRI correlation. Recently Sacco et al5 analyzed 33 patients with
LMS and described the MRI findings as abnormal in 20 of
22 patients in whom MRI was performed. However, they
failed to correlate the diverse clinical manifestations with
MRI findings, and a detailed clinical-MRI correlation
study remains to be reported. In the present study we
describe 33 patients with LMS in whom MRI showed
appropriate lesions and attempt to correlate their clinical
findings with the results of MRI.
Subjects and Methods
At Asan Medical Center (Seoul, South Korea), MRI scan
was performed in 37 patients with clinically suspected LMS
from June 1990 to December 1993. In this anatomicoclinical
correlation study, 4 patients were excluded: 2 with equivocal
lesions, 1 with additional pontine lesions, and 1 with bilateral
medullary lesions. The remaining 33 patients showed unilateral lesions mainly involving the dorsolateral portion of the
medulla oblongata. Some patients with lesions extending beReceived January 4, 1994; final revision received March 10,
1994; accepted March 25, 1994.
From the Departments of Neurology (J.S.K, J.H.L., M.C.L.)
and Radiology (D.C.S.), 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 134-600,
South Korea.
O 1994 American Heart Association, Inc.
Results
Neurological Symptoms and Signs
The patients' neurological symptoms and signs are
summarized in Fig 1. Vertigo/dizziness (30 [91%]), gait
1406
Stroke Vol 25, No 7 July 1994
No/Sex/Age RF V/D NS GA N/V DS HS HN FP HE SEN
+ + ++ + + +
2/M/52
+ - +
+ + + • - + -
+ - +
- + + + + + - < ?
3/M/60 HT.CD
4/M/64 HT.DM
+
-
++
+ «• + - J £
++
+
i^ '-
©
/j^i
+ • • Jj
t
<C)
6/M/55 HT.DM
* - ** - ** * * * * X -
7/M/58
HT
+ - +
8/M/68
HT
+ +• ++ + ++ + - + - jC
10/M/67
HT
+ *•+ + + + - * ,
+ •+ + + - -
+
+
t+
+*
+
Downloaded from http://stroke.ahajournals.org/ by guest on July 31, 2017
D M
13/F/47 HT.DM
+
*
- * + +*
- + +
+
+
t
+
.
+
*
"
"P
8
n
"
-
np
np
(.„£>
Ucl, an -
np
^ 3
Upl
+
np
*
"P
£
^ Q
^/^ Q
Uvm
P
-
{\JD
• + ++ - ++ + * • - 2L
ll/M/43 HT.HL.SM - • • • 12/M/58
5?
U 1
Ucl
5 /^k
C-£>
+ - -
Ucl
Ucl
^T\
(---<•>
5/M/56 HT, HL
9/M/59 HT.HL
Remark Cbll Angio
1
l/M/64 HT.SM
HT
MR1
Uvm
Ulg.Mpl Ucl.Mis -
np
np
-
+
* * * * " "
* *
* + - - X>
{ ^
Mvm
-
np
14/M/48 DM.SM.HL + * ++ * *
* - - - ,3L
£ )
Mel
-
-
15/M/63 HT.SM
+ ++ ++ + *+ + + + * j E ,
(fl
Mhe
- np
16/F/36
+ + • + +
+ +++ - - .
/ ^
Mpl.an
*
*
17/M/51 SM.HL
* - -
- *
- • - - ,|k
,O
Mel
-
np
18/F/63
+ + +
*
£)
Mpl
-
np
none
HT
(C) g
+
+
+
-
^
j?_.
-
jL
19/M/61 HT.CD.SM * - -
* -
+ • - - }<,
Q^l
Mis
- np
20/M/58 none
• • + •
+ -
. . . . f |t
£_J
Mpl
.
21/M/55 HT, DM.HL + + • + +
+ +
- • - - ^
C^
(Q
Mpl.Lls -
+ - ** * -
- • - - ^
O
(3
Mcl.Lls-
22/M/57 HT.DM
23/F/56 HT
t
...
....
24/F/71
HT
+
++
25/F/56
HL
• • • + - - - - -
V
^J
Lpl
26/F/59
HT
+ - * •
t
Ci C3 Mcl.Lls - np
JJ
^
(^
Mpl.Lls - np
+ -
. - - -
^
^\
Lcl
27/F/44 none
+ ++ ++ + -
- * * -
&
Q,
Lvm
28/F/52
HL
+ + +
.
{^
29/M/55
DM.HL
• • • •
•
"k.
,* \
(I)
>
30/F/64
HT
*
+
-
• * » « - -
- + -
-
-
-
+ -
-
-
np
9
• + • - - - - -
*
np
£
i.
+
np
Lls
-
np
Lpl. an
-
np
£J
Lls
-
np
-
np
np
^
-
* -
-
i}>.
O
Lls
3 2 / M / 6 2 HT. CD. SM • • • • • - -
-
* -
-
jL
€£>
Lvm
-
33/M/61
- + - -
J^>
L j
Lls
- np
31/F/65
HT
HT.SM
* +< ** -
• + • + - -
-
FIG 1. Chart showing clinical and radiological features of 33 patients. RF indicates risk factors; V/D, vertigo/dizziness; NS, nystagmus;
GA, gait ataxia; UN, nausea/vomiting; DS, dysphagia; HS, hoarseness; HN, Homer sign; FP, facial paresis; HE, hemiparesis; SEN,
sensory abnormality; MRI, magnetic resonance imaging; Cbll, cerebeliar lesion; Angio, angiographic vascular lesion; HT, hypertension;
SM, cigarette smoking; CD, cardiac disease; DM, diabetes mellitus; HL, hyperlipidemia; +, present (see "Subjects and Methods" for
more specific definitions); - , absent; C, contralateral to lesion; I, ipsilateral to lesion; U, upper; cl, classic; Ig, large; vm, ventromedial;
an, anterior; pi, posterolateral; M, middle; Is, lateral-superficial; he, hemi; L, lower; and np, not performed.
Kim et al Lateral Medullary Syndrome and MRI
1407
Downloaded from http://stroke.ahajournals.org/ by guest on July 31, 2017
Fra 2. Magnetic resonance Imaging showing characteristics of
medulla: upper medulla (top left), middle medulla (top right), and
lower medulla (bottom left).
ataxia (29 [88%]), nausea/vomiting (24 [73%]), nystagmus (22 [67%]), Horner sign (24 [73%]), dysphagia (20
[61%]), hoarseness (18 [55%]), and facial (28 [85%])
and hemibody (31 [94%]) sensory changes were frequent clinical manifestations. Mild facial paresis of the
central type on the side ipsilateral to the lesion was seen
in 12 patients (36%), and 4 had mild hemiparesis, 1 on
the side ipsilateral to the lesion. Although facial sensory
change ipsilateral to the lesion was usual, 9 patients
showed facial sensory dysfunction on the side contralateral to the lesion, and 1 had bilateral facial sensory
abnormalities. In 4 patients facial sensory change was
restricted to the ophthalmic division of trigeminal (VI)
area, and in 2 there was no facial sensory change. In 2
patients there was no definite sensory dysfunction in
either the face or the body.
Imaging and Vascular Studies
Eight patients had lesions in the upper medulla, 8 in
the middle medulla, and 9 in the lower medulla. Four
had lesions in the upper and middle medulla, and 4 in
the middle and lower medulla. The lesions in the upper
and the middle medulla were usually diagonal bandshaped and situated in the posterolateral portion of the
medulla. Diagonal band-shaped lesions sparing the
most posterolateral portion were most common and
therefore classified as the classic type (Fig 3, top panel).
Diagonal band-shaped lesions situated more ventromedially were classified as the ventromedial type (Fig 3,
top panel), which was defined when the center of the
lesion was located inside the medial half of a line drawn
as in Fig 3, top panel. Lesions encompassing the most
posterolateral surface of the medulla were designated
as posterolateral. However, a few lesions were large
enough to encompass the ventromedial and posterolateral part of the medulla and were designated as large. In
some patients (usually those with lower medullary lesions), the lesions were located in the lateral surface of
the medulla and were classified as the lateral-superficial
type (Fig 3, bottom panel). In a few patients, additional
or extended lesions were seen in the anterior half of the
medulla; these were classified as anterior and hemi
types, respectively. This classification was made by one
of the authors, who was blind to the patients' clinical
findings.
Twelve patients showed lesions in the upper medulla
(4 of them had concomitant middle medullary lesions).
Generally, the lesions in the upper medulla were thick
and diagonal band-shaped. They were classified as
classic in 4, classic and anterior in 1, ventromedial in 2,
large in 3, and posterolateral in 2. Sixteen had lesions in
the middle medulla (4 had lesions in the upper medulla
and 4 had lesions in the lower medulla concomitantly).
Lesions were classified as classic in 4, ventromedial in 1,
posterolateral in 6, posterolateral and anterior in 1,
hemi in 1, and lateral-superficial in 3. Thirteen had
lesions in the lower medulla. The lesions were most
often located superficially: lateral-superficial in 8, posterolateral in 1, posterolateral and anterior in 1, classic
in 1, and ventromedial in 2.
In addition to the medullary lesions, 7 patients
showed infarcts in the cerebellum. Fourteen had CT
scan before MRI examination, which universally failed
to localize medullary lesions but detected concomitant
cerebellar infarcts in 3 patients. Seven patients had
angiography, which showed vascular abnormalities in 4
1408
Stroke
Vol 25, No 7 July 1994
pyramid
medial lemniscus
inferior olive
ascending trigeminal tract
spinothalamic tract
descending trigeminal tract
restiform body
pyramid
Downloaded from http://stroke.ahajournals.org/ by guest on July 31, 2017
Fra 3. Schematic drawing of medulla (modified from Heines7)
showing important structures and
pattern of lesions (top, upper medulla; bottom, lower medulla. Diagonal stripes Indicate classic
type; vertical stripes, ventral; nonrandom dots, posterolateral; random dots, anterior; and horizontal
stripes, lateral-superficial.
ventral spinocerebellar tract
spinothalamic tract
nucleus ambiguus
descending trigeminal tract
dorsal spinocerebellar tract
patients: vertebral artery stenosis or occlusion in 3 and
severe basilar artery stenosis in 1.
Clinical-MRI Correlation
To elucidate the clinical difference between rostral
and caudal lesions, we divided the patients into three
groups according to rostrocaudal aspect of the lesion
identified by MRI.
through 33; n = 13). The patients tended to have lesions
in the superficial area. No patients had dysphagia or
hoarseness, except for 2 (patients 21 and 23) with
concomitant middle medullary lesion who reported
transient dysphagia. Vertigo and dizziness were noted
by aU and were usually severe. Gait ataxia, detected in
12 patients, was severe in 11. Six showed nystagmus on
forward gaze. Nine had nauseaA'omiting, and 9 showed
Horner sign. Facial paresis was observed in 1 patient.
Two (1 ventromedial, 1 posterolateral-anterior) showed
facial sensory change on the side contralateral to the
lesion.
Rostral Group
This group included patients with lesions in the upper
medulla or both upper and middle medulla (patients 1
through 12; n=12). All patients in the rostral group had
dysphagia and needed nasogastric tube insertion for feeding, and 5 of them had to use it for more than 3 months.
All patients exhibited hoarseness. Six patients had no
nystagmus, and only 1 had nystagmus on forward gaze.
Gait ataxia was present in 11 and was severe in 8. Homer
sign was present in 10 patients, and ipsilateral facial
paresis was observed in 10. Ten patients had vertigo/
dizziness; 8 had nauseaA'omiting. Four patients (2 ventromedial, 2 large) showed facial sensory change on the side
contralateral to the lesion. One (patient 11, classified as
large) showed bilateral facial sensory dysfunction.
Middle Group
This group included patients with middle medullary
lesions (patients 13 through 20; n=8). This group
exhibited intermediate characteristics. Six had dysphagia, but only 2 needed a nasogastric tube. Six had
hoarseness, 7 had vertigo/dizziness, and 7 reported
nauseaA'omiting. Homer sign and facial paresis were
seen in 5 and 1, respectively. Three patients (1 ventromedial, 1 hemi, and 1 classic) had facial sensory change
on the side contralateral to the lesion.
Caudal Group
This group included patients with lesions in the lower
medulla or lower and middle medulla (patients 21
The clinical characteristics of our patients are generally
similar to those described in recent clinical studies of
Discussion
Kim et al
Downloaded from http://stroke.ahajournals.org/ by guest on July 31, 2017
LMS.5'8 In our study we attempted to correlate the clinical
manifestations with MRI results. Although it is difficult to
classify the various lesions satisfactorily, we attempted to
divide the cases with reference to the rostrocaudal aspects
to elucidate possible clinical difference.
The most distinguishing rostrocaudal symptomatic difference was dysphagia, which was distinctly more severe in
the rostral group than in the caudal group. Patients with
middle medullary lesions showed an intermediate degree
of severity. The different degrees of severity of dysphagia
may be explained in several ways. Dysphagia in medullary
stroke is caused by involvement of the nucleus ambiguus,
a vertical columnar structure extending to the level of
pyramidal decussation.7 This structure, seen in the middle
portion of the medulla (Fig 3), may have been more
frequently involved in the rostral group because lesions in
this group were generally thick and tended to involve the
ventral portion of the medulla. The lesions of the caudal
group usually involved the superficial area and may have
spared the more medially located nucleus ambiguus. However, patients with deep lesions in the caudal group
(patients 27 and 32) also showed no dysphagia. Possibly
only a caudal part of the nucleus ambiguus, a portion not
directly related with visceral efferent fibers,9 may have
been involved in this group. Whatever the actual explanation, caudal group patients have a more benign prognosis
in terms of aspiration. As expected, hoarseness, another
symptom related to nucleus ambiguus involvement, was
also more marked in the rostral group than in the caudal
group.
Nystagmus, gait ataxia, and vertigo/dizziness were
apparently more severe in patients in the caudal group,
although the latter symptoms were not objectively
graded in this study. Nystagmus in LMS is attributed to
involvement of the vestibular nuclei or their connections
to the cerebellum,911 which begin at the caudal part of
the medial and inferior vestibular nuclei.9 A focal lesion
in this area was reported to cause severe vestibuloocular symptoms.12 The vestibulocerebellar pathway
runs through the juxtarestiform body, a part of the
inferior cerebellar peduncle, in the posterolateral medulla.9 These areas tended to be spared in the patients
with upper medullary lesions, among whom 6 of 8 did
not show nystagmus. Gait ataxia, a very common sign in
our series, is attributed to involvement of either the
restiform body or the spinocerebellar pathway.10'11 In
the lower medulla, both of these structures are located
in the lateral surface,7-9 which may have been frequently
involved in patients in the caudal group (Fig 3, bottom
panel). The involvement of the cerebellum, detected in
7 patients, does not appear to augment the severity of
gait ataxia.
The neural substrate for nausea and vomiting, common symptoms of LMS, is not clearly defined. Whereas
Peterman and Siekert13 suggested that nausea and
vomiting are attributed to lesions of the vestibular
nuclei, Currier et al10 stated that these symptoms are
related to involvement of the medullary vomiting center, which may be identical to the nucleus ambiguus. In
our series symptoms of nausea/vomiting were not specifically associated with the presence of dysphagia or
nystagmus. The neural substrate for these symptoms
may be related to both of the above structures. Horner
syndrome, a sign related to the descending sympathetic
Lateral Medullary Syndrome and MRI
1409
pathways in the lateral reticular formation,10 is also
common in our series regardless of lesion location.
Although dissociated sensory abnormality seen in
classic LMS is usual in our series, 9 patients showed
facial sensory change on the side contralateral to the
lesion. All had lesions involving the ventromedial or
anterior part of the medulla (ventromedial in 4, large in
2, hemi in 1, classic in 1, and posterolateral-anterior in
1), which would involve the ascending trigeminal sensory tract located in the medial-ventral portion of the
medulla 679 (Fig 3, top panel). One patient (patient 11)
had bilateral facial sensory change, probably because of
a wide lesion involving both the descending and ascending trigeminal sensory tract.11 Two (patients 19 and 25)
did not reveal any sensory abnormalities, probably
because of sparing of the spinothalamic and trigeminal
pathways. Three (patients 28, 30, and 31) showed
hemihypesthesia without facial sensory change. Facial
sensation was spared in 7 of 39 patients in the study of
Currier et al,10 who suggested that the descending
trigeminal sensory tract may be spared in ventrally
situated lesions. Our patients, however, had lateralsuperficial lesions in the lower medulla, suggesting that
the descending trigeminal tract located posteromedially
(Fig 3, bottom panel) may have been spared. Four of
our patients had facial sensory change restricted to the
VI area: 2 in the side ipsilateral and 2 in the side
contralateral to the lesions. Because the VI area is
located most ventrally in the descending trigeminal
tract, Currier et al10 thought that this sensory pattern
may be associated with a ventrally located lesion. However, the patients with ventromedial-type lesions did not
reveal this type of sensory change in our series, and the
mechanism of restricted facial sensory deficit in patients
7 and 17 remains unclear. Restricted sensory change of
the VI area on the side contralateral to the lesion
(patients 29 and 32) may be due to selective involvement
of the lateral part of the ascending trigeminal tract,
where the sensory fibers from the upper part of the face
are located.10
Facial paresis ipsilateral to the lesion was observed in
12 patients (36%) in our series. Fisher and Tapia14
reported an autopsy-proven case of LMS associated
with a severe peripheral type of facial paralysis, which
was caused by extension of the lesion to the lower pons,
involving intra-axial facial nerve fascicles. In our series
no patients showed obvious lesions in the pons, and all
had a mild, usually transient facial paresis of the central
type. Currier et al10 and Sacco et al5 noted weakness of
the facial muscles in 51% and 42% of their patients,
respectively, and suggested that aberrant, looping corticobulbar fibers15 may have been involved in these
patients. Most of our patients with facial paresis had
lesions in the rostral medulla, suggesting that the aberrant fibers, if they exist, may not descend to the level of
the lower medulla, although 1 patient (patient 27) with
a caudal lesion of the ventromedial type also showed
facial paresis. Finally, 4 of our patients showed mild
hemiparesis. All except 1 had lesions extending anteriorly, suggesting that the corticospinal tract was involved.
Of the 4,1 (patient 29) showed hemiparesis on the side
ipsilateral to the lesion. In this patient a coronal cut of
the MRI showed that the lesion extended into the upper
cervical cord (Fig 4), which probably involved the
pyramidal tract after decussation.
1410
Stroke Vol 25, No 7 July 1994
References
FIG 4. Patient 29. TV-weighted coronal imaging showing lesion
involving the upper cervical area lower than pyramidal decussatton.
Downloaded from http://stroke.ahajournals.org/ by guest on July 31, 2017
In conclusion, our study illustrates that the clinical
and topographic spectra of LMS are diverse, and MRI
analysis in rostrocaudal and dorsoventral aspects allows
us, although not unequivocally, to make clinical-MRI
correlations. Generally, the rostral lesions are diagonal
band-shaped and correlate with severe dysphagia,
hoarseness, and the presence of facial paresis, whereas
caudal lesions, usually involving lateral superficial areas,
appear to correlate with more marked nystagmus, vertigo, and gait ataxia. Nausea/vomiting and Horner sign
are common regardless of the lesion location. Lesions
extending ventromedially correlate with contralateral
facial sensory change, whereas anteriorly located lesions are associated with hemiparesis.
1. Lee BCP, Kneeland JB, Deck MDF, Cahill PT. Posterior fossa
lesion: magnetic resonance imaging. Radiology. 1984;153:137-143.
2. Kistler JP, Buonanno FS, DeWitt LD, Davis KR, Bray TJ, Fisher
CM. Vertebra-basilar posterior cerebral territory stroke: delineation by proton nuclear magnetic resonance imaging. Stroke.
1984;15:417-426.
3. Ross MA, Biller J, Adams HP, Dunn V. Magnetic resonance
imaging in Wallenberg's lateral medullary syndrome. Stroke. 1986;
17:542-545.
4. Bogousslavsky J, Fox AJ, Barnett HJM, Hachinski VC, Vinitski S,
Carey LS. Clinico-topographic correlation of small vertebrobasilar
infarct using magnetic resonance imaging. Stroke. 1986;17:929-938.
5. Sacco RL, Freddo L, Bello JA, Odel JG, Onesti ST, Mohr JP.
Wallenberg's lateral medullary syndrome: clinical-magnetic resonance imaging correlations. Arch NeuroL 1993;50:609-614.
6. Bradley WG Jr. MR of the brain stem: a practical approach.
Radiology. 1991;179:319-332.
7. Heines DE. Neuwanatomy: An Atlas of Structures, Sections and
Systems. 2nd ed. Berlin, Germany: Urban & Schwarzenberg;
1987:78-91.
8. Norrving B, Cronqvist S. Lateral medullary infarction: prognosis in
an unselected series. Neurology. 1991;41:244-248.
9. Carpenter MB, Sutin J. Human Neuroanatomy. 8th ed. Baltimore,
Md: Williams & Wilkins Co; 1983:315-357.
10. Currier RD, Giles CL, DeJong RN. Some comments on Wallenberg's lateral medullary syndrome. Neurology. 1961;l:778-792.
11. Caplan LR, Pessin MS, Mohr JP. Vertebrobasilar occlusive
disease. In: Barnett HJM, Mohr JP, Stein BM, Yatsu FM, eds.
Stroke: PathophysUAogy, Diagnosis, and Management. 2nd ed. New
York, NY: Churchill Livingstone, Inc; 1992:443-515.
12. Grant G. Infarction localization in a case of Wallenberg's syndrome: a neuroanatomical investigation with comments on
structures responsible for nystagmus. JHirnforsch. 1966;8:419-422.
13. Peterman AF, Siekert RG. The lateral medullary (Wallenberg)
syndrome: clinical features and prognosis. Med Gin North Am.
1960;ll:778-790.
14. Fisher CM, Tapia J. Lateral medullary infarction extending to the
lower pons. / Neurol Neurosurg Psychiatry. 1987;50:620-624.
15. Kuypers HGJM. Cortico-bulbar connections to the pons and lower
brainstem in man: an anatomical study. Bram. 1958;81:364-388.
Spectrum of lateral medullary syndrome. Correlation between clinical findings and
magnetic resonance imaging in 33 subjects.
J S Kim, J H Lee, D C Suh and M C Lee
Stroke. 1994;25:1405-1410
doi: 10.1161/01.STR.25.7.1405
Downloaded from http://stroke.ahajournals.org/ by guest on July 31, 2017
Stroke is published by the American Heart Association, 7272 Greenville Avenue, Dallas, TX 75231
Copyright © 1994 American Heart Association, Inc. All rights reserved.
Print ISSN: 0039-2499. Online ISSN: 1524-4628
The online version of this article, along with updated information and services, is located on the
World Wide Web at:
http://stroke.ahajournals.org/content/25/7/1405
Permissions: Requests for permissions to reproduce figures, tables, or portions of articles originally published in
Stroke can be obtained via RightsLink, a service of the Copyright Clearance Center, not the Editorial Office.
Once the online version of the published article for which permission is being requested is located, click Request
Permissions in the middle column of the Web page under Services. Further information about this process is
available in the Permissions and Rights Question and Answer document.
Reprints: Information about reprints can be found online at:
http://www.lww.com/reprints
Subscriptions: Information about subscribing to Stroke is online at:
http://stroke.ahajournals.org//subscriptions/