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j.jstrokecerebrovasdis.2018.05.040

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ARTICLE IN PRESS
Clinical Study on 3 Patients with Infarction of the Vermis/Tonsil
in the Cerebellum
D1X XKatsuhiko Ogawa, MD,
D2X X
* D3X XYutaka Suzuki, MD,
D4X X
† D5X XTakayoshi Akimoto, MD,
D6X X
*
D7X XAkihiko Morita, MD,
D8X X
* D9X XMakoto Hara, MD,
D10X X
* D1X XHirokazu Yoshihashi, MD,
D12X X
‡
D13X XSatoshi Kamei, MD,
D14X X
* and D15X XMasayoshi Soma, MD
D16X X †
Background: Infarction of the vermis and the tonsil in the cerebellum presents as
truncal and gait ataxia. Acute rotatory vertigo is often present in infarction of the
nodulus in the caudal vermis, which is closely associated with the vestibular pathway, but is minor in infarction of the rostral vermis. The rostral vermis receives
input from the dorsal spinocerebellar tract (DSCT) which conveys unconsciousness
proprioceptive signals from the ipsilateral lower trunk and leg. The present study
investigated the characteristics of infarction of the vermis and the tonsil. Patients
and Methods: Neuroradiological findings of 3 patients whose lesions were located in
the vermis or the tonsil were analyzed. Results: All lesions were located in the anterior lobe in the rostral vermis, the nodulus in the caudal vermis, or the tonsil. Truncal and gait ataxia were exhibited by 3 patients. Rotatory vertigo was exhibited by 2
patients whose lesions were located in the nodulus and the tonsil, but absent in a
patient with infarction of the anterior lobe. Lateropulsion opposite the lesion was
apparent in a patient with infarction of the tonsil. Gaze-evoked nystagmus was
observed in 2 patients with infarction of the nodulus and the tonsil.
Conclusions: The tonsil and the nodulus were considered to have a close relationship
with the vestibular pathway. Absence of rotatory vertigo indicated impairment of
the DSCT. Our data suggested that the cause of truncal and gait ataxia differed
between the rostral vermis and the caudal vermis/tonsil.
Key Words: Vermis infarction—nodulus—tonsil—nodulovestibular Purkinje
fibers—anterior lobe—dorsal spinocerebellar tract
© 2018 National Stroke Association. Published by Elsevier Inc. All rights reserved.
The vermis exists at the median zone in the cerebellum.1,2 Dysfunction of the vermis causes truncal and gait
ataxia, and is often accompanied by truncal lateropulsion.2,3 Magnetic resonance imaging (MRI) has made it
possible to detect a small infarct in the cerebellum
From the *Division of Neurology, Department of Medicine, Nihon
University School of Medicine, Tokyo, Japan; †Division of General
Medicine, Department of Medicine, Nihon University School of Medicine, Tokyo, Japan; and ‡Department of Neurology, Kobari General
Hospital, Chiba, Japan.
Received March 27, 2018; revision received May 1, 2018; accepted
May 25, 2018.
Address correspondence to Yutaka Suzuki, MD, Division of
General Medicine, Department of Medicine, Nihon University School
of Medicine, 30 -1 Oyaguchi-Kamimachi, Itabashi-ku, Tokyo 1738610, Japan. E-mail: suzuki.yutaka@nihon-u.ac.jp
1052-3057/$ - see front matter
© 2018 National Stroke Association. Published by Elsevier Inc. All
rights reserved.
https://doi.org/10.1016/j.jstrokecerebrovasdis.2018.05.040
including in the vermis.4 Infarction of the vermis has been
recently reported.5 9 In the previously reported
patients,5 9 the nodulus in the caudal vermis was most
commonly involved.5 9 Infarction of the nodulus presents
as acute rotatory vertigo and truncal and gait ataxia
including lateropulsion, whereas ataxia of the extremities
was slight or absent.5 9 Thus, neurological findings of
infarction of the nodulus mimicked those of peripheral
vestibulopathy, such as benign paroxysmal positional vertigo, and it was referred to as pseudo-labyrinthine disease
or isolated vascular vertigo.5 7,10 15 Additionally, infarction of the tonsil in the cerebellum, which demonstrated
rotatory vertigo, was reported.16 The tonsil is adjacent to
the caudal vermis and also supplied by the medial branch
of the posterior inferior cerebellar artery (mPICA) as the
caudal vermis.1,3 Furthermore, a patient with infarction of
the rostral vermis was reported to exhibit isolated lateropulsion without rotatory vertigo.17 Here, we assessed the
neurological characteristics for infarction of the vermis
Journal of Stroke and Cerebrovascular Diseases, Vol. &&, N0. && (&&), 2018: pp 1-7
1
ARTICLE IN PRESS
HTN, af
CE
Mild stenosis of
the bil VA/BA
¡
AD of the rt VA
A to A embolism DL
Moderate stenosis
of the bil VA
Moderate stenosis
of the rt VA
¡
Lateropulsion to the lt
side.
Lateralized to the lt side
after 2 steps walking
with assistance
¡
¡
rt tonsil
+ (Rotatory)
+ (rt)
+ (Rotatory)
+
+ (Rotatory)
¡
¡
¡
Vascular findings
Ataxia of the
extremities Nystagmus
Truncal and gait ataxia
+ (Dizziness) Unstable in normal walking and tandem gait
+ (Rotatory) Unstable in standing with
closed gait, Unstable in
wide-based gait
¡
+ (Dizziness) ¡
3/86/F
Three patients were enrolled in our study. Infarcts were
located in the anterior lobe in the rostral vermis on the left
side (patient 1) (Fig 1, A, B), in the nodulus in the caudal
2/22/M
Distribution of Infarcts
No./age/ Location of
Nausea/ Headache/
gender infarction Acute vertigo Vomit Neck pain Vertigo
Results (Table 1)
Neurological symptoms upon admission
Infarcts in the cerebellum were identified using 1.5-tesla
MRI (DWIs, fluid-attenuated inversion recovery imaging,
and T2-weighted imaging). The extent of infarcts was
measured on findings of T2-weighted images and DWIs.
Vascular findings for the posterior circulation were evaluated, based on results of magnetic resonance angiography
in 2 patients (patients 1, 3) and by 3-dimensional computed tomographic angiography in 1 (patient 2). The etiologies of infarction were comprised of (1) cardiogenic
embolism (CE) associated with emboligenic heart disease
such as atrial fibrillation (af), (2) atherothrombotic large
vessel disease (LVD) with angiographic evidence of moderate to severe stenotic and occluded arteries of the posterior circulation in the absence of emboligenic heart
disease, and (3) arterial dissection (AD) in the vertebral
artery (VA) or the basilar artery (BA). LVD was subdivided into branch atheromatous disease when moderate
to severe stenosis of the main trunk artery (the BA or the
VA) was adjacent to the lesions, or artery-to-artery (A to
A) embolism when moderate to severe stenosis was found
in the proximal region of the main trunk artery to the
lesions. Identification of AD was made when serrated
irregularity of the wall (string sign) was detected in the
VA or the BA in a patient with neck pain at onset. Small
vessel disease (SVD) was considered when CE or LVD
was not indicated.
Initial symptoms
Location of Infarcts and Vascular Findings
Table 1. Clinical findings for 3 patients with infarction of the vermis/tonsil in the cerebellum
We analyzed neurological and MRI findings of 2
patients with infarction of the vermis and 1 patient with
infarction of the tonsil in the cerebellum (age, 22-86 years;
male, n = 1). The elapsed time between the onset of the initial symptoms and MRI assessment ranged from 15 hours
to 2 days. Brain infarction was diagnosed, based on the
presence of a high-intensity area in diffusion-weighted
images (DWIs). The medical charts of the patients were
reviewed to identify initial symptoms, neurological findings upon admission, and vascular risk factors. A boardcertified specialist in neurology (K.O., Y.S., T.A., A.M., M.
H., H.Y., and S.K.) performed neurological examinations.
Nystagmus was assessed using the confrontation test.
Etiology
Characteristics of the Enrolled Patients (Table 1)
lt anterior
lobe
rt nodulus
Patients and Methods
1/66/F
Risk
factors
and the tonsil in the cerebellum, based on neuroradiological findings in patients whose lesions were located in
these areas.
Abbreviations: AD, arterial dissection; af, arterial fibrillation; A to A: artery to artery; BA, basilar artery; BAD, branch atheromatous disease, bil, bilateral; CE, cardiogenic embolism; DL, dyslipidemia; HTN, hypertension; lt, left; rt, right; VA, vertebral artery.
K. OGAWA ET AL.
2
ARTICLE IN PRESS
CEREBELLAR VERMIS/TONSIL INFARCTION
vermis on the right side (patient 2) (Fig 2, A-D), and in the
tonsil on the right side (patient 3) (Fig 3, A, B).
Initial Symptoms of the 3 Patients
Three patients exhibited acute vertigo at onset. The type
of vertigo was rotatory in 2 patients (patients 2, 3) and
dizziness in the other patient (patient 1). Neck pain on the
ipsilateral side of the lesion as well as nausea/vomiting
were presented by 1 patient at onset (patient 2).
Figure 1. An axial diffusion-weighted image and its schematic (A, B)
(patient 1). An abnormal high-intensity area was noted in the anterior lobe
in the rostral vermis on the left side.
3
Neurological Findings on Admission
Vertigo was still present in all 3 patients on admission.
The type of vertigo on admission was the same at onset in
all. Truncal ataxia was present in 2 patients (patients 2, 3).
Lateropulsion was identified in 1 patient (patient 3). The
direction of lateropulsion was to the opposite side of the
lesion (patient 3). Gait ataxia was exhibited by 3 patients.
Two patients were able to walk without assistance
(patients 1, 2). One patient was unstable during normal
walking and tandem gait (patient 1). Another patient
exhibited unstable wide-based gait (patient 2), which suggested that the gait ataxia in the 2 patients was not severe.
Severe gait ataxia was exhibited by 1 patient (patient 3).
This patient veered to the opposite direction of the lesion
after 2 to 3 steps while walking with assistance (patient 3).
No patients had ataxia of the extremities or ataxic speech.
Gaze-evoked nystagmus was demonstrated by 2 patients
(patients 2, 3) when looking to the side of the lesions
(toward the right). The type of nystagmus was horizontal
in patient 2 and horizontal/torsional in patient 3. Other
neurological findings were normal in 3 patients.
Vascular Findings, Etiology of Infarction, and Vascular
Risk Factors
The bilateral VAs demonstrated moderate stenosis;
however, the BA was normal in patient 1 whose lesion
was located in the rostral vermis (Fig 4). Accordingly, A
to A embolism was considered as the etiology. Moderate
stenosis with string sign was observed in the distal part
of the right VA in patient 2 whose lesion was located in
the right nodulus in the caudal vermis (Fig 5). In this
patient, AD was considered as the etiology because of
presence of neck pain at onset and string sign of the VA
ipsilateral to the lesion. Blood analysis for the antiphospholipid antibody, protein-c, and protein-s was negative
in this patient. The patient whose lesion was located in
the tonsil had accompanying af (patient 3), but the
degree of stenosis of the bilateral VAs and BA was mild
Figure 2. T2-weighted images and their schematics (patient 2). An axial
section showed an abnormal high-intensity area in the nodulus in the caudal
vermis on the right side (A, B). This lesion was also delineated in a coronal
section (C, D).
Figure 3. An axial diffusion-weighted image and its schematic (A, B)
(patient 3). An abnormal high-intensity area was noted in the tonsil on the
right side.
Figure 4. Magnetic resonance angiography (patient 1). Moderate stenosis
was observed in the bilateral vertebral arteries.
ARTICLE IN PRESS
K. OGAWA ET AL.
4
Figure 5. Three-dimensional computed tomographic angiography (patient
2). The distal part of the right vertebral artery noted moderate stenosis with
string sign (serrated irregularity of the wall), which indicated presence of
arterial dissection.
(Fig 6). Thus, CE was considered to be the etiology. Two
patients had vascular risk factors of hypertension (patient
3) and dyslipidemia (patient 1). No patients were suspected of having SVD.
Discussion
The cerebellum is supplied by the superior cerebellar
artery (SCA) in the rostral part and by the posterior inferior cerebellar artery (PICA) in the caudal part
(Fig 7).1,18,19 The SCA arises from the distal region of the
Figure 6. Magnetic resonance angiography (patient 3). Mild stenosis was
found in the bilateral vertebral arteries and the basilar artery.
BA,18,19 and the PICA arises from the distal region of the
VA as usual.18,19 The SCA and the PICA have 3 branches
each: the medial branch, the intermediate branch, and the
lateral branch (Fig 7).1 The vermis is supplied by 2 arteries: the medial branch of the superior cerebellar artery
(mSCA) (Fig 7) and the mPICA.1 The mPICA supplies the
caudal vermis including the nodulus, and the tonsil
(Fig 8).1,19
The vestibular signs of cerebellar infarction are caused
by involvement of the uvulo-nodular complex in the caudal vermis which is supplied by the mPICA (Fig 8).3,5,9
The clinical features mimic those of peripheral vestibulopathy because other neurological findings including ataxia
of the extremities are slight or absent.5 7,10 15 These cases
are referred to as isolated vascular vertigo.10 In infarction
of the territory of the anterior inferior cerebellar artery
(AICA), isolated vertigo with hearing loss and tinnitus
can occur due to ischemia of the labyrinthine artery originating from the AICA.10,11,20 In this situation, it is difficult
to differentiate between infarction of the territory in the
AICA and the labyrinthine disease, based solely on the
neurological findings because both the cochlear signs and
the vestibular signs are present.10,11,20 Two patients whose
lesions were located in the nodulus in the caudal vermis
or the tonsil (patients 2, 3) exhibited truncal and gait
ataxia and rotatory vertigo, without other neurological
findings, mimicking peripheral vestibulopathy. Infarction
of the vermis presenting as isolated vertigo has been
recently reported.5 9 In these reported patients,5 9 the
nodulus was most commonly involved. The vestibular
nucleus in the lower pons is comprised of 4 subnuclei
(superior, medial, lateral, and inferior subnuclei), and connects with the vestibule, the ipsilateral nodulus, and the
ipsilateral fastigual nucleus through neurofibers (Fig 9).21
Information from the vestibule approaches the 4 vestibular subnuclei in the lower pons via the vestibular ganglion.21 Part of the fibers directly from the vestibule
approach the nodulus without a junction in the vestibular
nucleus.21 Fibers from the superior and lateral subnuclei
in the vestibular nucleus component innervate the nodulus on the ipsilateral side,21 and then fibers from the nodulus approach the fastigual nucleus.21,22 The fastigual
nucleus innervates the bilateral vestibular nuclei.21,22
Additionally, the nodulus projects nodulovestibular Purkinje fibers to the ipsilateral inferior and medial subnuclei
in the vestibular nucleus, and exerts the inhibitory effects
on the vestibular nucleus (Fig 9).5,8,21,22 If the nodulus is
involved, the nodulovestibular Purkinje fibers may be
impaired,5,8 which leads to impairment in inhibition of
the medial and inferior vestibular subnuclei by the nodulus.5,22 This condition can cause lateropulsion to the opposite side of the lesion (Table 2). In our patient (patient
2),5,6,8,22 rotatory vertigo and truncal and gait ataxia were
observed, which suggested possibly involvement of the
nodulovestibular Purkinje fibers in the nodulus lesion,
although lateropulsion was absent.
ARTICLE IN PRESS
CEREBELLAR VERMIS/TONSIL INFARCTION
5
Figure 7. Schematic of the arterial supply to the brainstem and cerebellum from a lateral view (modified from the original figure by Goto1). The medial branch of
the superior cerebellar artery supplies the rostral part of the vermis.
Infarction of the tonsil in the cerebellum is rare.16 Only 1
patient with infarction of the tonsil has been reported to
date. This reported patient exhibited rotatory vertigo, but
lateropulsion was not apparent.16 Our patient with infarction of the tonsil (patient 3) had rotatory vertigo and lateropulsion to the opposite side of the lesion. This was
consistent with the typical symptoms of infarction of the
nodulus.5,6,8,22 There was a possibility that the tonsil
exerted inhibitory effects on the vestibular nucleus on the
ipsilateral side, similar with the nodulus (Table 2), and the
Figure 8. Schematic of the vermis and tonsil (modified from the original
figure by Goto1). The anterior lobe is located in the rostral vermis and comprises the central lobe and the culmen. The nodulus is located in the anteroinferior part of the vermis. The tonsil is adjacent to the nodulus and the
uvula.
disinhibitory effect caused by the tonsil lesion on the vestibular nucleus resulted in rotatory vertigo and lateropulsion to the opposite side of the lesion.
Truncal and gait ataxia were also presented by the
patient with infarction of the rostral vermis which is supplied by the mSCA, but rotatory vertigo was absent
(patient 1). This clinical feature is consistent with the lack
Figure 9. Schematic of vestibulocerebellar connections in the vestibular
pathway (modified from the original figure by England MA and Wakely
J21). The vestibular nucleus which is composed of the 4 subnuclei (superior,
medial, lateral, and inferior) is located in the lower pons. Information from
the vestibule approaches the vestibular nucleus via the vestibular ganglion.
The nodulus receives fibers from the superior and lateral vestibular subnuclei, and those from the vestibule directly project to a part of the nodulus.
The next fibers from the nodulus approach the ipsilateral fastigual nucleus.
The fastigual nucleus innervates the bilateral vestibular nuclei. The medial
and inferior vestibular subnuclei are innervated from the ipsilateral nodulus
through the inhibitory nodulovestibular Purkinje fibers.
ARTICLE IN PRESS
K. OGAWA ET AL.
The same side of the lesion
The opposite side of the lesion
The opposite side of the lesion
+
+
+
Abbreviations: PICA, posterior inferior cerebellar artery; SCA superior cerebellar artery.
+
+
+
¡
¡
¡
Rostral vermis (anterior lobe)
Caudal vermis (nodulus)
Tonsil
SCA
PICA
PICA
Dorsal spinocerebellar tract
Nodulovestibular Purkinje fibers
Fibers between tonsil and vestibular nucleus
¡
+
+
Truncal and
gait ataxia
Ataxia of the
extremities
Rotatory
vertigo
The impaired tract
The responsible
artery
Location
Table 2. Clinical characteristics of infarction of the vermis/tonsil in the cerebellum
Lateropulsion
Direction of the lateropulsion
6
of association between the vestibular pathway and the rostral vermis.2,23 Lee et al17 reported a patient with isolated
lateropulsion to the ipsilateral side of the lesion due to
infarction of the rostral vermis, and considered involvement of the dorsal spinocerebellar tract (DSCT) as a cause
of lateropulsion (Table 2). The DSCT conveys unconsciousness proprioceptive signals from the ipsilateral lower
trunk and leg.22,24,25 The DSCT travels the dorsolateral
surface of the caudal medulla and then enters the cerebellum through the inferior cerebellar peduncle, and finally
approaches the anterior lobe in the rostral vermis and the
gracile lobule on the ipsilateral side.17,24 26 In our patient
(patient 1), truncal and gait ataxia without rotatory vertigo
was observed. Involvement of the DSCT was considered
in this patient, although lateropulsion was not noted.
Calic et al4 previously reported the frequency, etiology,
and outcome of small cerebellar infarction. The size of the
lesions in our 3 patients was small. The lesions were confined and did not spread to the cerebellar hemisphere. In
this previous report,4 the main cause of small cerebellar
infarction was CE and LVD, not SVD. Based on this result,
Calic et al4 emphasized the need for investigation for a
cardiac source of embolism and vascular risk factors in
patients with small cerebellar infarction. In our study,
dyslipidemia was accompanied in patient 1 whose etiology was A to A embolism in LVD. The etiology in patient
3 was CE caused by af. These results were consistent with
the report of Calic et al.4 In contrast, infarction in patient 2
was juvenile-onset and occurred in the absence of vascular risk factors and emboligenic heart disease. AD of the
VA tends to occur in juvenile patients without vascular
risk factors,27,28 which was consistent with the clinical features in patient 2.
In conclusion, infarction of the rostral and caudal vermis commonly presented as truncal and gait ataxia in
common, but rotatory vertigo was absent in patients with
infarction of the rostral vermis. This result indicated the
difference in impaired fibers between the rostral and caudal vermis, and suggested a close relationship of the vestibular pathway with the nodulus. Infarction of the tonsil
caused lateropulsion to the opposite side of the lesion and
rotatory vertigo, which suggested that the tonsil exerted
an inhibitory effect on the vestibular nucleus on the ipsilateral side, similar with the nodulus.
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